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69 publications mentioning hsa-mir-153-2

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-153-2. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 315
Taken together, our study demonstrated that i) Nrf-2 was a target gene of miR-153 in GSCs, ii) miR-153 was down-regulated in GSCs, which led to radioresistance through up-regulation of Nrf-2 and GPx1, and iii) miR-153 overexpression decreased radioresistance and stemness of GSCs in vitro and in vivo. [score:11]
We found that miR-153 overexpression impaired the GSH system, increased ROS production, apoptosis and radiosensitivity, decreased neurosphere formation capacity and stem cell marker expression, and induced differentiation in GSCs by targeting Nrf-2. To identify the signaling pathways involved in miR-153 overexpression mediated differentiation of GSCs, we determined whether p38 MAPK signaling pathway was activated. [score:9]
These results demonstrated that miR-153 overexpression would indirectly impair the GSH system in GSCs through targeting Nrf-2. Figure 4 A. Real-time RT-PCR analysis of miR-153 expression in GSCs. [score:8]
These results demonstrated that miR-153 overexpression would indirectly impair the GSH system in GSCs through targeting Nrf-2. Figure 4 A. Real-time RT-PCR analysis of miR-153 expression in GSCs. [score:8]
MiR-153 is thought to be one of the brain-enriched miRs, which play crucial roles not only in the development and function of the central nervous system (CNS), but also in the pathogenesis of CNS disease, such as Parkinson's disease (PD) and Alzheimer's disease (AD) [40, 41]. [score:8]
As miRs are believed to inversely control mRNA translation, miR-153 were selected as a candidate miR targeting Nrf-2 and we speculated that reduced miR-153 might lead to the enhanced Nrf-2 expression in GSCs. [score:7]
Collectively, these data demonstrated that miR-153 expression was down-regulated in GSCs compared with that of non-GSCs glioma cells, which contributed to enhanced Nrf-2 expression resulting in activation of GPx1 transcription. [score:7]
In this study, Nrf-2 was identified as a target gene of miR-153 in GSCs by bio-informatic analysis, real-time PCR, and luciferase reporter assay, so the downregulation of miR-153 contributed to the elevated Nrf-2 expression in GSCs, at least in part. [score:7]
To investigate whether Nrf-2 overexpression could rescue stemness of GSCs with miR-153 overexpression, we detected the stem cell marker Bmi1 and differentiation marker GFAP expression by Western blot 48 h after Nrf-2 expression vectors transfection. [score:7]
To investigate whether Nrf-2 overexpression could rescue stemness and radioresistance of GSCs with miR-153 overexpression, we detected the stem cell marker expression and examined radiosensitivity of GSCs 48 h after Nrf-2 expression vectors transfection. [score:7]
Zhao et al. found that miR-153 was downregulated in CD133+ GSCs and miR-153 inhibited self-renewal ability of CD133+ GSCs and induced apoptosis [42]. [score:6]
MiR-153 overexpression suppressed Nrf-2 expression and Redox enzymes activity in GSCs. [score:6]
As shown in Figure 8B, Nrf-2 overexpression also rescued the decreased neurosphere formation capacity of GSCs resulting from miR-153 overexpression. [score:5]
Nrf-2 overexpression rescued the decreased stemness and radioresistance resulting from miR-153 overexpression in GSCs. [score:5]
Our results showed that miR-153 overexpression increased phosphorylated p38 and ATF2 and downstream differentiation markers in GSCs and these effects were almost totally reversed by a free radical scavenger NAC, suggesting miR-153 overexpression inducing GSCs differentiation through ROS -mediated activation of p38 MAPK pathway. [score:5]
The results indicated that Nrf-2 overexpression could rescue the decreased stemness and radioresistance resulting from miR-153 overexpression in GSCs. [score:5]
These findings suggest that miR-153/Nrf-2/GPx1 pathway play a important role in regulating radiosensitivity and stemness of GSCs via ROS and targeting the miR-153/Nrf-2/GPx1 axis could be a novel approach in development of therapeutic strategies against glioma. [score:5]
Nrf-2 overexpression rescued stemness and radioresistance of GSCs with miR-153 overexpression. [score:5]
Our results showed that Nrf-2 was a target gene of miR-153 in GSCs and low level of miR-153 rescued Nrf-2 expression leading to activation of GPx1 transcription and decreased ROS level, which contributed to radioresistance of GSCs. [score:5]
We employed lentiviral -mediated gene transfer technique to overexpress miR-153 in order to target Nrf-2 and analyzed phenotypic changes in GSCs. [score:5]
These results indicated that Nrf-2 overexpression could rescue the decreased stemness resulting from miR-153 overexpression in GSCs. [score:5]
As shown in Figure 3F, after miR-153 oligos were transfected into GSCs with the wild type reporter construct pGL3-Luc-Nrf-2, luciferase activity was significantly repressed compared with transfection of scramble oligos, whereas mutations in predicted target site of 3′-UTR of Nrf-2 gene abrogated the inhibition by miR-153 oligos. [score:5]
These results indicated that Nrf-2 overexpression could rescue the decreased radioresistance resulting from miR-153 overexpression in GSCs. [score:5]
To investigate whether Nrf-2 overexpression could rescue radioresistance of GSCs with miR-153 overexpression, we examined radiosensitivity by clonogenic assay 48 h after Nrf-2 expression vectors transfection. [score:4]
MiR-153 is significantly down-regulated in glioma compared with normal brain tissues and decreases cell proliferation and increases apoptosis by targeting B cell lymphoma 2 (Bcl-2) and myeloid cell leukemia sequence 1 (Mcl-1) genes in glioma cell lines [23]. [score:4]
These results suggest that Nrf-2 is a direct and robust target gene of miR-153 in GSCs. [score:4]
When 300 or 3, 000 cells were injected, the tumor incidence of GSCs with miR-153 overexpression decreased compared with that of GSCs expressing scramble sequence. [score:4]
B. The percentage of GSCs with miR-153 overexpression forming neurospheres. [score:3]
A. The diameters of neurospheres of GSCs with miR-153 overexpression plated at 100 cells per well in 96-well plates. [score:3]
As shown in Figure 7A, miR-153 overexpression increased phosphorylated p38 and ATF2 and differentiation marker GFAP, and caused FoxO3 activation as evidenced by its accumulation in the nucleus. [score:3]
These results indicated that miR-153 overexpression decreased stemness and induced differentiation through ROS -mediated activation of p38 MAPK in GSCs. [score:3]
The in vivo data showed that miR-153 overexpression could reduce tumor-initiating potential of GSCs and increase survival in mice bearing human GSCs. [score:3]
Figure 6 A. The diameters of neurospheres of GSCs with miR-153 overexpression plated at 100 cells per well in 96-well plates. [score:3]
Thus, to identify the signaling pathways involved in miR-153 overexpression mediated differentiation of GSCs, we first determined whether p38 MAPK signaling pathway was activated. [score:3]
C. Survival curves of GSCs/Lv-miR-153 transfected with Nrf-2 expression vectors. [score:3]
After transfection with p-Nrf-2, the tumor incidence of GSCs with miR-153 overexpression increased. [score:3]
The pivotal role of the microRNA-153/Nrf-2/GPx1 pathway in the control of radioresistance and stemness of GSCs demonstrated in this study suggested that the pathway might be a novel therapeutic target of GSCs. [score:3]
Nevertheless, after transfection with p-Nrf-2, the median survival of mice injected with GSCs with miR-153 overexpression decreased. [score:3]
B. The number of neurospheres per well of GSCs/Lv-miR-153 transfected with Nrf-2 expression vectors. [score:3]
Figure 5 A. Flow cytometric analysis of ROS formation in GSCs with miR-153 overexpression after exposure to ionizing radiation. [score:3]
These results indicated that miR-153 overexpression decreased the neurosphere formation capacity of GSCs. [score:3]
These in vivo data indicated that miR-153 overexpression could reduce tumorigenic capacity of GSCs and increase survival in mouse mo dels of human glioma. [score:3]
Moreover, N-acetylcysteine (NAC), which acts as a free radical scavenger by promoting intracellular biosynthesis of GSH, almost totally canceled the effect of p38 MAPK activation resulting from miR-153 overexpression. [score:3]
Representative photomicrographs showed that miR-153 overexpression decreased CD133 and nestin immunostatining and increases GFAP and Tuj-1 immunostaining in both stem cell lines (Figure 6C, 6D). [score:3]
C. Survival curves of GSCs with miR-153 overexpression. [score:3]
E. A putative miR-153 target site in the wild type and mutated 3′UTR of Nrf-2. F. Relative luciferase activity in GSCs transfected with pGL3-Luc vector containing wild type and mutated 3′UTR of Nrf-2. * P < 0.01 vs cells transfected with scramble oligos. [score:3]
To measure the effect of miR-153 overexpression on tumor formation, GSCs stably expressing miR-153 mature sequence or scramble sequence were intracranially implanted into immuno-compromised hosts. [score:3]
Gliomas were not observed in brains of mice injected with miR-153 overexpression GSCs irradiated by 8 Gy X-ray (Figure 9C). [score:3]
Moreover, miR-153 overexpression resulted in a slightly higher OER in GSCs. [score:3]
To experimentally determine whether miR-153 directly targets Nrf-2 by binding to its 3′ UTR sequence (Figure 3E), we employed luciferase reporter assays. [score:3]
A. Flow cytometric analysis of ROS formation in GSCs with miR-153 overexpression after exposure to ionizing radiation. [score:3]
Meanwhile, the stem cell markers, Bmi1 and nestin, were decreased in GSCs with miR-153 overexpression. [score:3]
B. Flow cytometric analysis of ROS formation in GSCs with miR-153 overexpression in the presence and absence of an antioxidant N-acetylcysteine (NAC). [score:3]
The target GSCs were infected with viruses encoding either miR-153 or scramble sequence and selected using puromycin. [score:3]
It is clear that GSCs with miR-153 overexpression were more radiosensitive than GSCs with stable integration of scramble sequence under normoxia or hypoxic conditions. [score:3]
A. Real-time RT-PCR analysis of miR-153 expression in GSCs. [score:3]
As shown in Figure 7B, miR-153 overexpression increased ROS formation in GSCs, which was abrogated in the presence of NAC. [score:3]
As a result, the GSH/GSSG ratio, an indicator of the cellular health, was significantly lower in GSCs with miR-153 overexpression. [score:3]
For all cell numbers transplanted, the median survival of mice injected with GSCs was increased with miR-153 overexpression. [score:3]
These results indicated that miR-153 overexpression decreased stemness and induced differentiation in GSCs. [score:3]
The 3′UTR of Nrf-2 gene contains a putative miR-153-target site: 5′-CTTTATAAGTAATTCTA TGCAA-3′. [score:3]
ROS generation was significantly increased in GSCs with miR-153 overexpression, whereas ROS generation in GSCs with stable integration of scramble sequence showed no obvious change 1 h after 8 Gy X-ray irradiation, as shown in Figure 5A. [score:3]
As shown in Figure 4D, GSH was significantly decreased, while GSSG was significantly increased in GSCs with miR-153 overexpression. [score:3]
We used lentiviral transduction to overexpress miR-153 (Figure 4A) and evaluate its effects in GPx1 expression and activity in GSCs. [score:3]
In addition, miR-153 overexpression reduced tumorigenic capacity of GSCs and increased survival in mice bearing human GSCs. [score:3]
Kaplan-Meier curves further demonstrate significant increases in survival with introduction of miR-153 overexpression and/or 8 Gy X-ray irradiation (Figure 9B). [score:3]
The apoptosis of GSCs induced by miR-153 even in the absence of radiation might result from targeting B cell lymphoma 2 (Bcl-2) and myeloid cell leukemia sequence 1 (Mcl-1) genes, which has been reported by previous study [23]. [score:3]
Moreover, we found that miR-153 overexpression resulted in radiosensitization of GSCs as well as decreased stemness and increased differentiation through ROS -mediated activation of p38 MAPK in GSCs. [score:3]
For initial experiments, we performed an in vivo limiting dilution assay with GSCs stably expressing miR-153 mature sequence or scramble sequence. [score:2]
MiR-153 overexpression activated p38 MAPK signaling pathway via ROS in GSCs. [score:2]
MiR-153 overexpression decreased stemness and induced differentiation through ROS -mediated activation of p38 MAPK in GSCs. [score:2]
MiR-153 overexpression increased ROS production, apoptosis and radiosensitivity of GSCs. [score:2]
MiR-153 overexpression decreased the neurosphere formation capacity and stemness of GSCs. [score:2]
MiR-153 overexpression decreased stemness and induced differentiation in GSCs. [score:2]
MiR-153 overexpression increased ROS production, apoptosis and radiosensitivity in GSCs. [score:2]
As shown in Figure 4B, Nrf-2 and GPx1 protein expression were significantly decreased in GSCs with stable integration of miR-153 compared with that of control cells. [score:2]
MiR-153 overexpression reduces tumorigenic capacity of GSCs. [score:2]
Our results thus far determined an important role for miR-153 in GSC stemness, survival, and radioresistance in vitro, but the ultimate goal of any cancer stem cell–directed therapy is to provide therapeutic benefit in vivo. [score:2]
Our results showed that the average apoptotic rate of GSCs with miR-153 overexpression irradiated by 0 or 5 Gy X-ray were significantly increased compared with those of control cells (Figure 5B). [score:2]
To generate the respective viruses, 293T cells were transfected with the lentiviral vector, pGLV-miR-153-GFP or pGLV-scr-GFP, and the packaging plasmid PG-P1-VSVG, PG-P2-REV and PG-P3-RRE according to standard protocols. [score:1]
For intracranial implantation, 36 h after irradiation with 8 Gy X-ray, GSCs/Lv-scr, GSCs/Lv-miR-153 and GSCs/Lv-miR-153+p-Nrf-2 cells were counted and the indicated numbers of GSCs were implanted into the right frontal lobes of 6–8-week-old female athymic nude mice (Experimental Animals Center of Shanghai Institute of Life Science, Shanghai, China). [score:1]
GSCs with stable integration of the miR-153 mature sequence or scramble sequence were generated through lentiviral -mediated gene transfer [48]. [score:1]
Twenty four hours later, 20 nM of miR-153 oligos (5′-UUGCAUAGUCACAAAAGUGAUC-3′) or scramble oligos (5′-UUCUC CGAACGUGUCACGUTT-3′) (GenePharma Co. [score:1]
[#] P < 0.01 vs miR-153. [score:1]
However, little is known about the molecular mechanisms of miR-153 functions in GSCs. [score:1]
Cells with stable integration of miR-153 were plated 24 h prior to transfection. [score:1]
We therefore evaluated the ability of miR-153 overexpression to increase the survival of immuno-compromised mice bearing intracranially implanted human GSCs. [score:1]
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2
[+] score: 263
Other miRNAs from this paper: hsa-mir-153-1
miRNA vectors, including miR-153 expression vector (HmiR0039-MR04), the control vector for miR-153 (CmiR0001-MR04), miR-153 inhibitor (HmiR-AN0214-AM04) and the negative control for the miR-153 inhibitor (CmiR-AN0001-AM04) were purchased from GeneCopoeia (Guangzhou, China). [score:7]
As assessed by RT-qPCR, the expression of miR-153 was overexpressed by miR-153 expression vector in MIAPaCa-2 cells (P<0.05, Fig. 3A). [score:7]
In these cases, SNAI1 expression was detected in 75.0% (30/40) of the PDAC samples with a low expression of miR-153, whereas only 42.5% (17/40) of the PDAC specimens with a high expression of miR-153 showed a positive SNAI1 signal (P<0.05, Fig. 5B). [score:7]
SNAI1 is identified as a functional target of miR-153 and is downregulated in PDAC specimens. [score:6]
Additionally, we found that the upregulation of miR-153 inhibited cell migration and invasion in MIAPaCa-2 cells. [score:6]
In conclusion, we found that miR-153 is downregulated in PDAC and its low expression is associated with poor prognostic features. [score:6]
MiR-153 high: value of expression > the median value; miR-153 low: value of expression < the median value. [score:5]
Overexpression of miR-153 promoted cell cycle transition and cell proliferation by inhibiting phosphatase and tensin homolog deleted on chromosome 10 (PTEN) in prostate cancer (17). [score:5]
The association between miR-153 expression and clinicopathological variables of PDAC patients are presented in Table I. of the statistical analysis revealed that, miR-153 was expressed at prominent lower levels in patients with lymph node metastasis, tumor recurrence, poor tumor differentiation and advanced tumor stage (P<0.05, respectively). [score:5]
A reduced expression of miR-153 has been observed in ovarian tumors and its low expression is correlated with FIGO grade 3 and advanced clinical stage, suggesting it is of potential importance as a diagnostic biomarker (10). [score:5]
miR-153 inhibits cell proliferation and induces apoptosis by targeting B-cell lymphoma 2 (Bcl-2) and myeloid cell leukemia sequence-1 (Mcl-1) in GBM cells (3– 9). [score:5]
miR-153 promoted invasiveness indirectly by inducing matrix metal-loprotease enzyme 9 (MMP9) production, whereas drug resistance was mediated directly by inhibiting the forkhead transcription factor forkhead box O3a (FOXO3a) (18). [score:5]
These results suggest that the downregulation of miR-153 plays critical roles in PDAC progression and development. [score:5]
miR-153 signifi-cantly inhibited the luciferase activity of SNAI1 containing a wt 3′-UTR, but did not suppress the activity of SNAI1 with a mt 3′-UTR (P<0.05, Fig. 4C and D). [score:5]
Consequently, we suggest that miR-153 inhibits cell migration and invasion by targeting SNAI1 in PDAC. [score:5]
The 3′-untranslated region (3′-UTR) sequence of SNAI1, predicted to interact with miR-153 or a mutated sequence within the predicted target sites, was produced and inserted into the XbaI and FseI sites of the pGL3 control vector (Promega, Madison, WI, USA). [score:5]
Mechanistically, we suggest that miR-153 inhibits PDAC cell migration and invasion by suppressing SNAI1. [score:5]
miR-153 expression is significantly lower in lung cancer tissues as compared with adjacent tissues and exerted antitumor activity in lung cancer by targeting protein kinase B (AKT) (14). [score:4]
miR-153 downregulated AsPC-1 cells, which was confirmed by RT-qPCR (P<0.05, Fig. 3C). [score:4]
For the reporter assay, MIAPaCa-2 cells were seeded in 24-well plates and transfected with the above constructs and miR-153 expression vector, miR-153 inhibitor, control vector or negative control. [score:4]
We found that upregulation of miR-153 led to a significant reduction of cell migration in MIAPaCa-2 cells (P<0.05, Fig. 3B). [score:4]
PDAC patients with a low expression of miR-153 had an evidently lower 3-year overall survival (OS) as compared with those with a high expression of miR-153 (P=0.041, Fig. 2). [score:4]
Previous studies reported that miR-153 was a novel regulator of EMT by targeting SNAI1 and ZEB2 in human epithelial cancers (12). [score:4]
The down-regulation of miR-153 promotes epithelial-mesenchymal transition (EMT) via SNAI1 and ZEB2. [score:4]
SNAI1 mRNA and protein levels were significantly reduced by upregulation of miR-153 in MIAPaCa-2 cells (P<0.05, respectively, Fig. 4A and B). [score:4]
To investigate the role of miR-153 in PDAC, miR-153 was upregulated in the MIAPaCa-2 PDAC cell line via expression of plasmid transfection. [score:4]
As expected, downregulation of miR-153 obviously promoted AsPC-1 cell migration and invasion (P<0.05, respectively, Fig. 3D). [score:4]
By contrast, the downregulation of miR-153 increased the number of migrated and invaded AsPC-1 cells. [score:4]
SNAI1 was also validated as a direct functional target of miR-153 in PDAC. [score:4]
miR-153 inhibits PDAC cell migration and invasion in vitro. [score:3]
Our data indicated that the level of miR-153 expression in PDAC tissues was significantly lower than that in normal pancreas tissues. [score:3]
Moreover, miR-153 expression is an independent prognostic marker for predicting 3-year survival of PDAC patients. [score:3]
These data suggest that miR-153 inhibits PDAC cell migration and invasion. [score:3]
However, miR-153 was found to be overexpressed in endome-trial, prostate and colorectal cancer (16– 18). [score:3]
The relative expression of miR-153 was shown as the fold difference relative to U6 (20). [score:3]
We then determined the expression of miR-153 in 80 cases of PDAC tissues and 30 cases of normal pancreas tissues. [score:3]
Our results showed that an impaired expression of miR-153 was observed in PDAC and it may be a potential prognostic biomarker for PDAC patients. [score:3]
Additional studies were performed to identify the molecular mechanisms by which miR-153 inhibited cell migration and invasion in PDAC. [score:3]
The expression of miR-153 in 80 cases of PDAC tissues was determined by RT-qPCR. [score:3]
Furthermore, miR-153 reduced the number of migrated and invaded non-small-cell lung cancer (NSCLC) cells by targeting the dynamic change of adamalysin 19 (ADAM19) (15). [score:3]
Furthermore, it was shown that patients with a low expression of miR-153 were associated with shorter recurrence-free survival (RFS) (P=0.039, Fig. 2). [score:3]
indicated that miR-153 was expressed at significantly lower levels in PDAC patients with lymph node metastasis, poor tumor differentiation, tumor recurrence and advanced TNM tumor stage. [score:3]
Thus, the expression of miR-153 was impaired in PDAC. [score:3]
Initially, we assessed the expression of miR-153 in a normal human pancreatic duct epithelial cell line (HPDE6-C7) and five PDAC cell lines (PANC-1, MIAPaCa-2, BxPC-3, AsPC-1 and PL45). [score:3]
of a clinical analysis have indicated that a low expression level of miR-153 was significantly associated with metastasis and poor prognosis in oral cancer patients (12). [score:3]
MIAPaCa-2 cells that were transfected with miR-153 and control vectors were subjected to RT-qPCR and western blotting for SNAI1 expression. [score:3]
Expression of miR-153 in human PDAC cells and tissue samples. [score:3]
Thus, our data strongly suggested that SNAI1 is a target of miR-153 in PDAC. [score:3]
In vitro studies demonstrate that miR-153 inhibits PDAC cell migration and invasion. [score:3]
We then detected the expression status of miR-153 in samples of surgically resected PDAC tissues and normal pancreas tissues. [score:3]
A significant inverse correlation between miR-153 and SNAI1 expression was also observed in PDAC tissues. [score:3]
The above mentioned studies indicate that miR-153 is a tumor suppressive miRNA. [score:3]
The expression of miR-153 in glioblastoma (GBM) is significantly lower than that in non-neoplastic brain tissue. [score:3]
Furthermore, Spearman’s correlation analysis indicated that miR-153 was inversely correlated with SNAI1 expression in PDAC tissues (r=−0.563, P<0.001). [score:3]
Thus, miR-153 inhibited cell migration and invasion in PDAC. [score:3]
Notably, the multivariate Cox regression analysis indicated that miR-153 expression was an independent factor for predicting the 3-year OS of PDAC patients (P=0.038, Table II). [score:3]
Altogether, these results suggest that miR-153 expression is critical for determination of prognosis in PDAC patients. [score:3]
The univariate and multivariate Cox regression analysis indicated that miR-153 expression was an independent prognostic factor for predicting OS of PDAC patients. [score:3]
Our data demonstrate that the low expression of miR-153 was correlated with a significant shorter 3-year OS and RFS for PDAC patients. [score:3]
Furthermore, as determined by Transwell invasion assays, the number of invaded MIAPaCa-2 cells was significantly decreased after miR-153 overexpression (P<0.05, Fig. 3B). [score:2]
To further demonstrate that SNAI1 was directly targeted by miR-153 in PDAC cells, we investigated whether the miR-153 directly interacted with the 3′-UTR of SNAI1 mRNA using a dual-luciferase reporter assay. [score:2]
Therefore, the functional significance of miR-153 in cancer development and progression seem to be cancer-type specific. [score:2]
The results suggest that, miR-153 inversely regulated SNAI1 abundance in PDAC cells. [score:2]
The expression of miR-153 was considered as either low (n=40) or high (n=40) according to the cut-off value, which was defined as the median of the cohort. [score:2]
Taken together, we considered that miR-153 potentially acts as a clinical biomarker, and may also be a therapeutic target in PDAC. [score:2]
The median value of miR-153 expression was considered as the threshold. [score:2]
In the present study, a reduced expression of miR-153 was observed in PDAC cell lines as compared with a normal human pancreatic duct epithelial cell line. [score:2]
Clinical significance of miR-153 in PDAC patients. [score:1]
miR-153 sensitizes leukemia cells to As2O3 -induced apoptosis (11). [score:1]
In the present study, the expression levels of miR-153 were measured by RT-qPCR in human PDAC cell lines and tissues. [score:1]
Furthermore, the prognostic value of miR-153 was determined by the Kaplan-Meier estimation. [score:1]
When anti-miR-153 was transfected, an increase in luciferase activity of wt SNAI1 3′-UTR was observed. [score:1]
However, the clinical and prognostic significance of miR-153 in human PDAC has not been elucidated. [score:1]
However, the role of miR-153 in PDAC remains to be determined. [score:1]
In breast cancer, miR-153 reduces cell proliferation and viability and induces apoptosis in MDA-MB-231 cells (13). [score:1]
These data indicated that miR-153 is a potent biomarker for predicting the prognosis of PDAC patients. [score:1]
We also investigated the clini-copathological significance of miR-153 expression in PDAC. [score:1]
Recently, miR-153 was identified as a robust biomarker of oral cancer with a high positive predictive value (12). [score:1]
The Kaplan-Meier survival analysis was performed to determine the prognostic value of miR-153 in PDAC patients. [score:1]
As measured by RT-qPCR, the relative expression of miR-153 in PDAC cell lines was significantly lower than that in the HPDE6-C7 (P<0.05, Fig. 1A). [score:1]
In the present study, we identified a new role of miR-153 in PDAC. [score:1]
In addition, a univariate Cox regression analysis indicated that clinicopathological characteristics, including tumor differentiation and stage, lymph node metastasis, tumor recurrence and miR-153 expression, were significantly associated with OS (P<0.05, respectively, Table II). [score:1]
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3
[+] score: 251
We found that the expression of adipokine Serpin A12 (SERPINA12) (Table 1, spot 5) is down-regulated in response to miR-153-3p overexpression whilst the pyruvate dehydrogenase complex beta subunit (PDHB) (Table 1, spot 2), a key enzyme linking the glycolytic pathway to the TCA cycle, is up-regulated (Table 1) [47]. [score:11]
miR-153 overexpression in HEK293 cells downregulate SNCA whilst miR-205 overexpression in HEK293 cells has been shown to downregulate LRRK2 [8, 9]. [score:11]
We found that miR-153-3p overexpression leads to an up-regulation of peroxiredoxin 2 (PRDX2) (Table 1, spot 1) whilst miR-153-3p inhibition results in peroxiredoxin-4 (PRDX4) precursor up-regulation (Table 1, spot 9). [score:11]
In response to miR-153-3p inhibition cofilin-1 was down-regulated (Table 1, spot 32), verified by western blot analysis (Fig 5B), whilst miR-205-5p overexpression resulted in cofilin-1 up-regulation (Table 1, spot 18). [score:11]
The stress -induced phosphoprotein 1 (STIP1) (Table 1, spot 4) is also up-regulated in response to the miR-153-3p mimic whilst the expression of mortalin (Heat shock 70kDa protein 9-HSPA9) (Table 1, spot 6) is down-regulated. [score:9]
Numbers (16–33) represent differentially expressed protein spots identified by MS, reported in Table 1. Overexpression of miR-153-3p resulted in up-regulation of proteasome subunit alpha type-1 isoform 2 (PSMA1) (Table 1, spot 4; S2 Fig). [score:8]
miR-153-3p overexpression also resulted in the up-regulation of High mobility group protein B1 (HMGB1) (Table 1, spot 3), involved in remo deling chromatin affecting gene expression (S3 Table) [48]. [score:8]
Transfections were performed, in triplicate, with scrambled control mimic, miR-153-3p mimic, miR-205-5p mimic, scrambled control hairpin inhibitor, miR-153-3p hairpin inhibitor and miR-205 hairpin inhibitor, all mirVana [TM] (Life Technologies), at a final concentration of 20 nM. [score:7]
We also found that 14-3-3 protein epsilon (14-3-3E) (Table 1, spot 15), involved in cell cycle regulation, PI3-Akt signaling, Hippo signaling, Neurotrophin signaling, and viral carcinogenesis (Fig 4), is down-regulated in response to miR-153-3p inhibition [26]. [score:7]
In response to altered levels of miR-153-3p seven protein spots were up-regulated whilst eight protein spots were down-regulated (Fig 2, Table 1). [score:7]
In contrast, alpha-enolase is down-regulated in response to miR-153-3p inhibition (Table 1). [score:6]
Inhibition of miR-153-3p also results in the up-regulation of the calcium activated chloride channel family member 4 (CLCA4) (Table 1, spot 9). [score:6]
Overexpression of miR-153-3p resulted in up-regulation of proteasome subunit alpha type-1 isoform 2 (PSMA1) (Table 1, spot 4; S2 Fig). [score:6]
Glucose stimulation increases miR-153 expression and miR-153 expression is reduced in PTPRN2 (Protein tyrosine phosphatase receptor type N polypeptide 2) mouse knockout mo dels [46]. [score:6]
In response to miR-153-3p inhibition we identified Nucleoside diphosphate Kinase B (Nm23) (Table 1, spot 10) and tumor suppressor alpha-enolase (Table 1, spot 11), two cell cycle regulatory proteins [38, 39]. [score:6]
To verify the up-regulation of HMGB1 in response to miR-153-3p overexpression we performed western blot analysis (Fig 5A). [score:6]
We also found that cathepsin Z (CTSZ) (Table 1, spot 13) is down-regulated in response to miR-153-3p inhibition. [score:6]
In terms of PD, miR-7/miR-153 and miR-205-5p have been shown to down-regulate SNCA and LRRK2, respectively whilst DJ-1 and Parkin are regulated by miR-34b/c [8, 9, 10]. [score:5]
In aging mouse brains cathepsin is upregulated, impairing neuronal survival and neuritogenesis, indicating that miR-153-3p may regulate cathepsin levels to maintain a healthy neuronal population [22]. [score:5]
This suggests that the proteins identified in this study represent a combination of direct and indirect targets of miR-153-3p and miR-205-5p. [score:5]
Overexpression and inhibition of miR-153-3p and miR-205-5p and their effect on cell viability in SH-SY5Y cells. [score:5]
Overexpression and inhibition of miR-153-3p and miR-205-5p in SH-SY5Y cells. [score:5]
miR-153-3p was successfully overexpressed using miR-153-3p mimic and inhibited using miR-153-3p antagomir in SH-SY5Y cells (Fig 1A and 1B). [score:5]
Interestingly, cofilin-1 (CFL1) (Table 1, spot 14), which decreases in abundance as a result of miR-153-3p inhibition, is shown to act as glucocorticoid receptor inhibitor [50]. [score:5]
Similar to miR-153-3p, miR-205-5p also down-regulates Serpin A12 (Table 1, spot 26). [score:4]
Protein association network showing interconnecting relationships between miR-153-3p and miR-205-5p target proteins through key regulatory pathways. [score:4]
This indicates that miR-153-3p may up-regulate PFDN2 in response to increased levels of misfolded proteins as a neuroprotective mechanism. [score:4]
Several of the protein targets identified are associated with neuronal processes and key regulatory pathways, indicating that miR-153-3p and miR-205-5p are involved in a wide variety of biological processes. [score:4]
S2 Fig Proteasome subunit alpha type-1 isoform 2 (PSMA1) (regulated by miR-153-3p and miR-205-5p) and proteasome subunit p42 (PSMC6) (regulated by miR-205-5p) are integral parts of the 26S proteosome. [score:3]
miR-153-3p inhibition results in increased abundance of Nm23 (Fig 2, spot 10), known as a transcriptional activator of c-myc [40]. [score:3]
miR-153-3p overexpression also resulted in increase abundance of Prefolding subunit 2 (PFDN2) (Table 1, spot 7), which transfers misfolded proteins to chaperonin ensuring proper folding [21]. [score:3]
Combined these results indicate that miR-153-3p and miR-205-5p may play a role in cell proliferation and migration involving various target proteins. [score:3]
Numbers (16–33) represent differentially expressed protein spots identified by MS, reported in Table 1. We identified thirty-three protein spots that showed significant abundance changes (fold change > 1.4, n = 3, p-value < 0.05) between control transfected and miR-153-3p/miR-205-5p -transfected SH-SY5Y cells. [score:3]
Our data indicates that both miR-205-5p and miR-153-3p influence direct and peripheral processes associated with neurodegenerative disorders, providing clues towards the possible regulation of key pathways (S4 Table, Fig 4). [score:3]
0143969.g001 Fig 1(A-B) Semi-quantitative RT-PCR analysis showing miR-153-3p expression levels in response to mimic (A) and antagomir (B) transfections. [score:3]
Numbers (16–33) represent differentially expressed protein spots identified by MS, reported in Table 1. We identified thirty-three protein spots that showed significant abundance changes (fold change > 1.4, n = 3, p-value < 0.05) between control transfected and miR-153-3p/miR-205-5p -transfected SH-SY5Y cells. [score:3]
CLCA4 inhibition by miR-153-3p may contribute to neuroprotection. [score:3]
Verification of differentially expressed proteins by Western blot analysis and ROS changes in response to miR-153-3p and miR-205-5p. [score:3]
Indeed, overexpression of miR-153-3p and miR-205-5p causes significant ROS reduction (Fig 5E). [score:3]
The aim of this study was to combine microRNA and proteomics technologies to identify new miR-153-3p and miR-205-5p targets in neuronal SH-SY5Y cells. [score:3]
We next sought to identify additional targets of miR-153-3p and miR-205-5p in SH-SY5Y cells using analysis. [score:3]
The targets of miR-153-3p and miR-205-5p were used as input queries for the Partek Genomics Suite software, version 6.6 (Partek) to perform Gene ontology (GO) analysis and generate interactive maps and pathways. [score:3]
Regulation of key neuronal processes by miR-153-3p and miR-205-5p. [score:2]
Collectively, miR-153-3p and miR-205-5p appears to regulate proteins involved in metabolic pathways and in particular carbohydrate metabolism (S4 Table). [score:2]
Peroxiredoxins are regulated by both miR-153-3p and miR205-5p. [score:2]
Cellular processes and pathway analysis of the differentially regulated proteins in response to mimics and antagomirs of miR-153-3p and miR-205-5p. [score:2]
List of differentially regulated proteins in SH-SY5Y cells in response to mimics and antagomirs of miR-153-3p and miR-205-5p. [score:2]
miR-153-3p and miR-205-5p have roles in regulating proteins involved in metabolic pathways. [score:2]
miR-153-3p and miR-205-5p alter known cell cycle regulators. [score:2]
The regulation of PRDXs by miR-153-3p and miR-205-5p suggest that miR-153-3p and miR-205-5p may affect cellular ROS levels. [score:2]
We performed comparative analysis comparing control mimic and control antagomir transfected cells with cells transfected with the miR-153-3p mimic and the miR-153-3p antagomir, respectively (Fig 2). [score:1]
However, before performing analysis we showed that miR-153-3p and miR-205-5p transfections had no significant effect on SH-SY5Y cell viability ensuring that any observed protein changes were due to changes in miR-153-3p and miR-205-5p levels (Fig 1D). [score:1]
We verified the miR-153-3p- and miR-205-5p -mediated increase in PRDX2 by western blot analysis (Fig 5A and 5C). [score:1]
Western blot analysis showing effect of miR-153-3p mimic on (A) PRDX2 and HMGB1 levels (B) effect of miR-153-3p antagomir on Cfl1 levels, (C) effect of miR-205-5p mimic on PRDX2, NACA and Cfl1 levels, (D) effect of miR-205-5p antagomir on NACA and Cfl1 levels. [score:1]
0143969.g002 Fig 2Two-dimensional gels of control mimic, miR-153-3p mimic, control antagomir and miR-153-3p antagomir transfected cells. [score:1]
Altered levels of miR-153-3p and miR-205-5p results in protein changes associated with a spectrum of biological processes. [score:1]
Two-dimensional gels of control mimic, miR-153-3p mimic, control antagomir and miR-153-3p antagomir transfected cells. [score:1]
Combined this indicate that miR-153-3p and miR205-5p influence PRDX levels, which may affect ROS levels (Fig 5F). [score:1]
0143969.g005 Fig 5Western blot analysis showing effect of miR-153-3p mimic on (A) PRDX2 and HMGB1 levels (B) effect of miR-153-3p antagomir on Cfl1 levels, (C) effect of miR-205-5p mimic on PRDX2, NACA and Cfl1 levels, (D) effect of miR-205-5p antagomir on NACA and Cfl1 levels. [score:1]
MicroRNA biology is complex and we have shown that miR-153-3p and miR-205-5p influences the abundance of numerous proteins integral to many biological processes in neuroblastoma cells (Fig 4, S3 Table). [score:1]
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4
[+] score: 246
Other miRNAs from this paper: mmu-mir-153, hsa-mir-153-1
The results above suggest that Rictor is a target gene of miR-153, and overexpression of miR-153 will lead to Rictor downregulation and p-Akt Ser473 inhibition in glioma cells. [score:10]
Our results suggest that miR-153 downregulation could be the reason of Rictor upregulation and mTORC2 over-activation in human glioma cells. [score:7]
In human glioma tissues and cells, miR-153 downregulation was negatively correlated with Rictor upregulation and mTORC2 (p-Akt Ser473) over-activation. [score:7]
3.1. miR-153 downregulation correlates with Rictor upregulation in multiple human glioma tissues and cell lines. [score:7]
We next wanted to know if miR-153 downregulation was the reason of Rictor upregulation in glioma cells. [score:7]
These results indicated that miR-153 downregulation could be the reason of Rictor upregulation and mTORC2 over-activation in glioma cells. [score:7]
Together, we showed that miR-153 downregulation could be the reason of Rictor upregulation and mTORC2 over-activation in glioma cells. [score:7]
Note that miR-153 downregulation and Rictor upregulation were most dramatic in U87MG cells and U373MG cells (Fig 1E–1G), these two cell lines were chosen for further studies. [score:7]
Importantly, exogenous overexpression of miR-153 downregulated Rictor and decreased p-Akt Ser473 in glioma cells. [score:6]
Real-time PCR results confirmed miR-153 upregulation (Fig 5E) and Rictor mRNA depletion (Fig 5F) in miR-153 -expressing tumors (at Week-5, n = 3 for each). [score:6]
miR-153 expression clearly downregulated Rictor mRNA in U87MG cells (Fig 2B). [score:6]
Thus far, we have shown that miR-153 downregulated Rictor and inhibited glioma cell growth in vitro. [score:6]
These results indicate that miR-153 over -expression -mediated anti-glioma cell activity is likely mediated via downregulating Rictor. [score:6]
Overexpression of miR-153 -induced anti-glioma cell activity is possibly via downregulating Rictor. [score:6]
Importantly, our in vivo studies showed that miR-153 downregulated Rictor/p-Akt Ser473, and potently inhibited U87MG tumor growth in nude mice. [score:6]
Meanwhile, significant growth inhibition and apoptosis activation were observed in the miR-153 -expressing glioma cells. [score:5]
First, we show that microRNA-153 (miR-153) selectively targets the 3’ untranslated regions (UTRs) of Rictor mRNA (Fig 1A). [score:5]
First, MTT results in Fig 3A and 3B showed that miR-153 overexpression significantly inhibited growth of U87MG and U373MG cells. [score:5]
Fig 5A showed that the average volume of miR-153 -expressing U87MG tumors was much smaller than that of the miR-C -expressing U87MG tumors. [score:5]
3.3. miR-153 overexpression inhibits glioma cell growth, and activates cell apoptosis. [score:5]
These results showed that cells with Rictor shRNA showed similar phenotypes (growth inhibition and apoptosis activation) as cells with miR-153 overexpression. [score:5]
Together, these results demonstrated that miR-153 over -expression inhibited U87MG tumor growth in vivo. [score:5]
Recent evidences have indicated that miR-153 was dramatically downregulated in several cancer cells [31, 32]. [score:4]
3.4. miR-153 -induced anti-glioma cell activity is mediated via downregulating Rictor. [score:4]
Since Rictor upregulation and mTORC2 over-activation are important for glioma cell growth and apoptosis-resistance [15], we then tested the potential role of miR-153 on glioma cell functions. [score:4]
Further, miR-153 -induced anti-glioma cell activity is possibly through downregulating Rictor. [score:4]
Meanwhile, the number of U87MG/U373MG colonies was decreased sharply after forced miR-153 expression (Fig 3C and 3D). [score:3]
We also analyzed expression of miR-153 and Rictor in the U87MG tumors. [score:3]
Real-time PCR results demonstrated that miR-153 level was dramatically downregulated in glioma tissues (“Glioma”), as compared to its level in the surrounding normal brain tissues (“Normal”) (Fig 1B). [score:3]
Intriguingly, in Rictor-silenced glioma cells, miR-153 expression failed to further decrease cell growth or increase cell apoptosis. [score:3]
pre-miR-153 construct was introduced into U87MG cells to establish miR-153 -expressing cell line (See Methods). [score:3]
miR-153 was first discovered as one of the several brain-specific miRNAs, based on analysis of expression profile of over one hundred miRNAs in adult organs [30]. [score:3]
Expressions of miR-153 (B), Rictor mRNA (C) as well as Rictor protein (D, vs. [score:3]
These results indicated that miR-153 overexpression exerted anti-growth and pro-apoptosis activity against glioma cells. [score:3]
When analyzing cell apoptosis, we detected a clear apoptosis activation in miR-153 -expressing U87MG cells (Fig 3E) and U373MG cells (Fig 3F). [score:3]
Next, we tested miR-153 and Rictor expressions in human glioma cells. [score:3]
These results [31, 32] have implied that miR-153 could be a tumor suppressor. [score:3]
Rictor is a target of miR-153 in glioma cells. [score:3]
One key finding of this study is that Rictor might be a key target gene of miR-153 in glioma cells. [score:3]
To test this hypothesis, we again overexpressed miR-153 in Rictor-silenced U87MG cells (Fig 4G). [score:3]
Expressions of miR-153 (E), Rictor mRNA (F) as well as Rictor protein (G) and p-Akt (G) in primary human astrocytes (“Astrocytes”) and established glioma cell lines (T98G,U373MG, U251MG and U87MG) were shown. [score:3]
Stable U87MG cells (2 × 10 [6] cells per mouse) expressing miR-153 or miR-C were s. c. injected into the nude mice, and xenografted tumors were established. [score:3]
Indeed, forced expression of miR-153 failed to further affect U87MG cell growth (Fig 4G) or apoptosis (Fig 4I) in these cells. [score:3]
Tian [24]) to generate miR-153 expression construct. [score:3]
Further, in grade IV (GBM multiforme) human gliomas, miR-153 expression appeared to be depleted [31, 32]. [score:3]
Real-time PCR results in Fig 2A confirmed miR-153 overexpression in the stable U87MG cells. [score:3]
If Rictor is the main target of miR-153 in glioma cells, miR-153’s activity against glioma cells should be diminished in Rictor-silenced cells. [score:3]
2.10. miR-153 overexpression. [score:3]
Therefore, Rictor should be the primary target of miR-153 in mediating its anti-glioma cell activity. [score:3]
miR-153 -expressing U87MG cells (“miR-153”) or miR-C -expressing U87MG cells (“miR-C”) were inoculated into the nude mice (13 mice per group), tumor volumes (A) and mice body weights (D) were recorded weekly; Estimated daily tumor growth was calculated (B); Mice survival at week-7 was also presented (C, summarizing of three-set repeats). [score:3]
Stable U87MG cells expressing miR-153, microRNA-control (“miR-C”) or empty vector (“pSuper-puro”) were subjected to real-time PCR assay of miR-153 (A) and Rictor mRNA (B). [score:2]
Rictor shRNA -expressing stable U87MG cells were transfected with miR-153 or microRNA-control (“miR-C”), miR-153 expression (G, Real-time PCR assay), cell growth (E, MTT assay) and apoptosis (F, Histone DNA ELISA assay) in these cells were tested. [score:2]
Relative Rictor mRNA (A) and miRNA-153 (C) expression in stable U87MG cells with scramble control shRNA (“shRNA-C”) or Rictor shRNA (“shRNA-Rictor”) was tested by Real-time PCR assay. [score:2]
At week-5, three xenografted U87MG tumors per group were isolated, miR-153 (E) and Rictor mRNA (F) expressions in the fresh tissues were tested by real-time PCR assay; Bars stand for mean ± SD. [score:2]
miR-153 expression in the stable cells was tested by real-time PCR assay. [score:2]
At week-7, the mice bearing miR-153 U87MG tumors were all alive, but the majority of mice with miR-C tumors were already dead (Fig 5C). [score:1]
0156915.g005 Fig 5The anti-glioma activity by miR-153 in vivo. [score:1]
For transfection, glioma cells were seeded onto 6-well plates at 50–60% confluence, which were then transfected with miR-153 construct (0.25 μg/ml) via Lipofectamine 2000 reagents (Invitrogen, Shanghai, China). [score:1]
In the current study, we identified a potential anti-Rictor miRNA: microRNA-153 (miR-153). [score:1]
Stable U87MG cells bearing miR-153 or miR-C were subcutaneously (s. c. ) injected into the right flanks of 4-week-old female nude mice (each mouse: 2 × 10 [6] cells in 200 µl of Matrigel). [score:1]
Finally, we tested miR-153’s activity on glioma cell growth in vivo. [score:1]
The anti-glioma activity by miR-153 in vivo. [score:1]
The level of miR-153 was obviously not affected by Rictor shRNA (Fig 4C). [score:1]
The anti-glioma activity by miR-153 in vivoFinally, we tested miR-153’s activity on glioma cell growth in vivo. [score:1]
Pre-miR-153 (see sequence in [23]) was sub-cloned into pSuper-puromycin vector (a gift from Dr. [score:1]
Average daily tumor growth results further confirmed the anti-glioma activity by miR-153 in vivo (Fig 5B). [score:1]
miR-153 (-3p) and its putative binding sequence in the 3’-UTR of Rictor mRNA (A). [score:1]
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5
[+] score: 199
Other miRNAs from this paper: hsa-mir-153-1
Overexpression of miR-153 inhibited oral tumor cell metastasis via directly targeting SNAI1and ZEB2, acting as a tumor suppressor gene in glioblastoma stem cells[24]. [score:10]
miR-153 overexpression can inhibit the expression of p-SMAD2, p-SMAD3, EGFR and IGFBP-3 expression, which are the downstream signaling molecules of TGF-β. [score:9]
Moreover, transforming growth factor (TGF)-β2 (TGF-β2) was confirmed as a new direct target of miR-153 in osteosarcoma, and miR-153 may suppress tumor growth and invasion by repressing the expression of TGF-β2. [score:8]
Recently, Yuan et al. also found that miR-153 played a tumor suppressive role in lung cancer by suppressing AKT expression[22]. [score:7]
TGF-β enhanced the mRNA and protein expression of IGFBP-3 and EGFR; meanwhile, following the miRNA-153 mimic treatment, EGFR and IGFBP-3 proteins and mRNAs were downregulated in the MG-63 cell line (Fig. 4B, C and D). [score:6]
These results suggest that miR-153 might act as a tumor suppressor gene whose down-regulation contributes to the progression and metastasis of osteosarcoma. [score:6]
This conclusion is supported by the following reasons: complementary sequence of miR-153 is identified in the 3’UTR of TGF-β2 mRNA; miR-153 overexpression led to a reduction at both mRNA and protein level of TGF-β2; reintroduction of miR-153inhibited 3’UTR luciferase report activity of TGF-β2and this effect was abolished by mutation of the miR-153 seed binding site. [score:6]
In the present study, the expression of miR-153 is down-regulated in osteosarcoma tissues and cell lines. [score:6]
Overexpression of miR-153 inhibited osteosarcoma cell proliferation and invasion. [score:5]
Moreover, miRNA-153 overexpression repressed the p-SMAD2, p-SMAD3, EGFR and IGFBP-3 expression. [score:5]
Overexpression of miR-153 resulted in inhibition of osteosarcoma cell proliferation and invasion. [score:5]
demonstrated that overexpression of miR-153 inhibited osteosarcoma cell proliferation and invasion. [score:5]
Furthermore, invasion analysis showed that miR-153 overexpression inhibited the invasive abilities of MG-63 cells (Fig. 2C). [score:5]
However, upregulation of miR-153 promoted colorectal cancer progression by increasing cell proliferation and down regulating PTEN [23, 28]. [score:5]
p-SMAD2, p-SMAD3, EGFR and IGFBP-3 protein expression were downregulated with the treatment of miRNA-153 compared with scramble (Fig. 4A). [score:5]
This was consistent with previous findings that overexpression of miR-153 suppressed glioblastoma (GBM) cell proliferation and GBM stem cell growth. [score:5]
These results indicate that miR-153 may function as a tumor suppressor partly by repressing TGF-β2 expression in osteosarcoma. [score:5]
The ectopic expression of miR-153 suppressed cell proliferation and invasion in osteosarcoma cells. [score:5]
Overexpression of miR-153 can also suppress TGF-β2 protein levels (Fig. 3D). [score:5]
MiR-153 overexpression repressed the p-SMAD2, p-SMAD3, EGFR and IGFBP-3 expression. [score:4]
TGF-β2 was a direct target of miR-153 in osteosarcoma cells. [score:4]
MiR-153 Overexpression repressed the p-SMAD2, p-SMAD3, EGFR and IGFBP-3 expression. [score:4]
In conclusion, we supposed that miR-153 played significant role in osteosarcoma development and might be a promising therapeutic target for osteosarcoma. [score:4]
Taken together, we demonstrated that miR-153 was downregulated in osteosarcoma cell lines and tissues. [score:4]
In the present study, the expression of miR-153 was down regulated in osteosarcoma cells and tissues. [score:4]
Furthermore, TGF-β2 is identified as a direct target of miR-153. [score:4]
We also showed that miR-153 was down-regulated in the osteosarcoma cell lines in vitro. [score:4]
Forced expression of miR-153 represses cell proliferation and invasion in MG-63 cells. [score:3]
0119225.g004 Fig 4 The MG-63 was treated in serum-free medium in the presence and absence of TGF-β (50 ng/ml), scramble, or miRNA-153 mimic for 24 h. (A) Expression of p-SMAD2, t-SMAD2, p-SMAD3 and t-SMAD3 was detected using western blotting. [score:3]
When miR-153 mimic and TGF-β was added into MG-63 cells, miR-153 mimic inhibited the TGF-β -induced osteosarcoma cell proliferation and invasion (Fig. 5A and B). [score:3]
The expression of miR-153 was normalized to U6 snRNA. [score:3]
Increased expression of miR-153 was confirmed using qRT-PCR (Fig. 2A). [score:3]
0119225.g001 Fig 1 (A) The miR-153 expression was determined by qRT-PCR in 20 paired osteosarcoma tissues and adjacent noncancerous tissues. [score:3]
TGF-β2 was predicted to be a target of miR-153 (Fig. 3A). [score:3]
The mRNA level of TGF-β2 was inhibited in the miR-153 mimic group (Fig. 3B). [score:3]
0119225.g002 Fig 2. (A) qRT-PCR analysis of miR-153 expression after the transfection of miR-153 mimics or scramble or no treat. [score:3]
Therefore, miR-153 may serve as a therapeutic target in osteosarcoma patients. [score:3]
The ability of miR-153 to target TGF-β2in our data may provide one mechanism of post-transcriptional control of TGF-β2. [score:3]
The MG-63 was treated in serum-free medium in the presence and absence of TGF-β (50 ng/ml), scramble, or miRNA-153 mimic for 24 h. (A) Expression of p-SMAD2, t-SMAD2, p-SMAD3 and t-SMAD3 was detected using western blotting. [score:3]
MiR-153 significantly suppressed the luciferase activity of WT 3’UTR, but not the MUT 3’UTR of TGF-β2 in MG-63 cells (Fig. 3C). [score:2]
0119225.g003 Fig 3. (A) Computer prediction of miR-153 binding sites in the 3’UTR of human TGF-β2 gene. [score:1]
Moreover, miR-153 is also involved in TGF-β -induced tumor proliferation and invasion. [score:1]
miR-153 was decreased in osteosarcoma tissues and cell line. [score:1]
miR-153 is involved in TGF-β -induced osteosarcoma cell proliferation and invasion. [score:1]
Increasing studies have shown that miR-153 is involved in the progression of many cancers, including breast cancer, glioblastoma, ovarian, oral, colorectal, lung and prostate cancer[20– 25]. [score:1]
Further investigation revealed that TGF-β2 was a potential target of miR-153. [score:1]
The MG-63 was treated in serum-free medium in the presence and absence of TGF-β (50 ng/ml), scramble, or miRNA-153 mimic. [score:1]
In our study, we investigated the expression of miR-153 in osteosarcoma clinical samples and identified that miR-153 was decreased in the osteosarcoma tissues. [score:1]
The role or molecular mechanism of miR-153 in osteosarcoma is still unknown. [score:1]
We further studied the functional roles of miRNA-153 in TGF-β signaling pathways. [score:1]
Previous studies have showed that miR-153 is involved in the progression of various cancers, including breast cancer, glioblastoma, ovarian, oral, colorectal, lung and prostate cancer[20– 25]. [score:1]
Subsequently, cells were transfected with 20 nM miR-153 mimics or scramble, 10 ng pGL3 and pGL3-TGF-β2–3’UTR or pGL3-TGF-β2–3’UTR Mut plasmid per well using Lipofectamine 2000, according to the manufacturer’s protocol. [score:1]
miR-153 was decreased in osteosarcoma tissues and cell lines. [score:1]
To our knowledge, no information is available on the role or molecular mechanism of miR-153 in osteosarcoma. [score:1]
0119225.g005 Fig 5. The MG-63 was treated in serum-free medium in the presence and absence of TGF-β (50 ng/ml), scramble, or miRNA-153 mimic. [score:1]
These dual effects of miR-153 may be attributed to organ-specific actions and its different cellular contexts in tumors. [score:1]
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6
[+] score: 172
Importantly, we found that systemic delivery of miR-153 antagomir up-regulated WWOX protein levels and inhibited expression of Wnt signaling target genes, including c-myc and Cyclin D1 (Figure 5C–5D). [score:10]
On the other hand, overexpression of miR-153 significantly inhibited the proliferation and migration, and promoted apoptosis of lung cancer cells, through suppression of AKT expression [35]. [score:9]
First, overexpression of miR-153 promoted, while its antisense inhibited the transcriptional activity of β-catenin and expression of its down-stream target genes. [score:9]
Besides, up-regulation of miR-153 promotes cell proliferation via suppression of the PTEN tumor suppressor gene in human prostate cancer [33]. [score:8]
At the molecular level, our luciferase reporter and analysis found that miR-153 could suppress WWOX expression through targeting its 3′-UTR region. [score:7]
In agreement, a dramatic up-regulation of WWOX was observed in cells with miR-153 inhibition (Figure 3C and Supplementary Figure 1B). [score:6]
Notably, we found that overexpression of miR-153 mimics resulted in a substantial increase of reporter activity (Figure 1A), which was accompanied by the up-regulation of Cyclin A, Cyclin D1, Cyclin E and C-myc, as well as the reduction of p21, leading to an increased cell cycle progression, cell proliferation and colony formation (Figure 1B–1F). [score:6]
In addition, we observed a reduced protein levels of WWOX and p21, an increased expression of Cyclin D1 by miR-153 overexpression (Figure 4C), suggesting that miR-153 could also promote tumor growth in vivo. [score:5]
To this end, bioinformatics software (TargetScan) was employed to identify potential target genes for miR-153. [score:5]
As expected, inhibition of miR-153 dramatically suppressed HCC growth and size (Figure 5A–5B). [score:5]
In agreement, inhibition of miR-153 by its antisense oligos led to a suppression of β-catenin activity (Figure 2A). [score:5]
In agreement, we found that overexpression of miR-153 mimics promoted, while its antisense inhibited the nuclear localization of Dvl-2 protein (Supplementary Figure 2A–2B). [score:5]
To understand how miR-153 regulates WWOX expression, the luciferase reporter plasmids containing the 3′-UTR of WWOX was co -transfected with miR-153 mimics or antisense. [score:4]
It has been reported that miR-153 was down-regulated and correlated significantly with advanced clinical stage in ovarian cancers [32], suggesting that miR-153 might be of potential importance as diagnostic biomarkers. [score:4]
However, the molecular determinants of miR-153 up-regulation in HCC tissues remain to be determined. [score:4]
Third, miR-153 was up-regulated in HCC tissues and correlated with poor survival of patients. [score:4]
The expression levels of Cyclin A, Cyclin D1, Cyclin E, C-myc and p21 were also affected by miR-153 antisense (Figure 2B–2C), accompanied with a reduction of cell growth and colony formation (Figure 2D–2F). [score:3]
Mutations were introduced in potential miR-153 binding sites using the QuikChange site-directed mutagenesis Kit (Stratagene, USA). [score:3]
MicroRNA-153 regulates β-catenin activation through suppression of WWOX. [score:3]
Figure 6 (A) miR-153 expression was determined by real-time PCR in human HCC tissues and adjacent normal tissues. [score:3]
Transfection of miR-153 mimics resulted in a reduced WWOX protein expression (Figure 3B and Supplementary Figure 1A). [score:3]
Next, we examined the mechanisms underlying the inhibitory effect of miR-153 on β-catenin -dependent gene transcription. [score:3]
Therefore, miR-153 could either act as an onco-miRNA or a tumor suppressor in human cancers, which might be dependent on cellular context. [score:3]
5.0 × 10 [6] HepG2 cells stably expressing miR-153 or negative control (miR-NC) were injected subcutaneously to the skin under the front legs of the mouse. [score:3]
To further demonstrate its function, we tested if forced expression of miR-153 promotes the ability of HepG2 cells to form xenograft tumors in nude mice. [score:3]
Next, we asked whether miR-153 inhibition has therapeutic and preventive effects for HCC using a murine liver cancer mo del. [score:3]
As a result, WWOX overexpression reversed the oncogenic roles of miR-153 (Supplementary Figure 3B–3C), underlining the specific importance of the WWOX for miR-153 action in the cell proliferation. [score:3]
MicroRNA-153 promotes HCC growth in vivoTo further demonstrate its function, we tested if forced expression of miR-153 promotes the ability of HepG2 cells to form xenograft tumors in nude mice. [score:3]
Among which, we found that WWOX, harbored a potential miR-153 binding site in its 3′-untranslated region (3′-UTR) (Figure 3A). [score:3]
Systematic administration of MicroRNA-153 suppresses HCC development in C57BL/6 mice. [score:3]
As expected, miR-153 was significantly up-regulated in HCC tissues, compared with adjacent normal tissues (Figure 6A). [score:3]
MicroRNA-153 regulates WWOX expression. [score:3]
As a result, the tumor volume and weight were markedly increased in miR-153 -overexpressed tumors compared to control tumors (Figure 4A–4B). [score:2]
To further investigate whether the deregulated abundant miR-153 correlates with the survival of HCC patients, expression levels of miR-153 were determined in HCC and matched non-cancerous tissues. [score:2]
As shown in the Supplementary Figure 4, expression levels of miR-153 gradually increased in C57BL/6 mice treated with DEN, compared with vehicle controls. [score:2]
Second, miR-153 could regulate cell proliferation and tumor growth in vitro and in vivo. [score:2]
In the present study, we performed a MicroRNA -based genetic screen, which revealed a novel diversion in β-catenin signaling triggered by miR-153 in HCC development. [score:2]
In the present study, our data showed that miR-153 could be a novel and important regulator of β-catenin signaling in HCC. [score:2]
MicroRNA-153 antisense inhibits β-catenin signaling. [score:2]
Taken together, in the present study, our results highlight the roles of miR-153 in the regulation of HCC. [score:2]
Moreover, miR-153 supports colorectal cancer progression via pleiotropic effects that enhance invasion and chemotherapeutic resistance [34]. [score:1]
Our results further indicate that miR-153-medicated activation of β-catenin may play an important role in the HCC progression. [score:1]
Figure 2 (A) HepG2 cells transiently transfected with the TopFlash–FopFlash and miR-153 antisense (AS) or NC for 36 hr. [score:1]
Figure 5 (A–B) Number of HCC tumors/liver (A) and tumor size (mm [3]) (B) in NC-, and miR-153 antigomir -treated mice. [score:1]
Furthermore, mutagenesis of the seed sequence abolished the effects of miR-153 mimics or antisense on WWOX activity (Figure 3D). [score:1]
Figure 4 (A–B) HepG2 cells stably transfected with miR-153 or negative control (NC) were injected into nude mice (n = 6–8 for each group) and followed up for tumorigenesis. [score:1]
To further verify the functional connection between miR-153 and WWOX, HepG2 cells were transfected with adenovirus containing WWOX or GFP as a negative control (Supplementary Figure 3A). [score:1]
Mice were systemically administrated with miR-NC or miR-153 antagomir at week 28. [score:1]
Cells were transfected with 100 ng of wild-type 3′-UTR-reporter or mutant constructs together with miR-153 mimics, antisenseor negative control (NC). [score:1]
miR-153 mimics and antisense were purchased from Ambion Company (Invitrogen, USA). [score:1]
Based on this finding, we treated mice with systemically administration of miR-NC or miR-153 antagomir at week 28. [score:1]
Kaplan-Meier analysis further revealed that low miR-153 level in HCC tissues significantly correlated with the markedly reduced tumor-free survival and overall survival of HCC patients (Figure 6B–6C). [score:1]
[1 to 20 of 52 sentences]
7
[+] score: 147
In-silico Prediction of Target miRNAs against Human Nrf2 and Experimental Validation of Nrf2 Downregulation by Forced Expression of miR144, miR153, miR27a and miR142-5pNrf2, an essential transcription factor for regulating both basal and inducible expression of diverse cytoprotective genes [26], [27] has been recently demonstrated to be regulated by miR144 and miR28 in non-neuronal mo dels [22], [23]. [score:12]
Individual overexpression of miR144, miR153, miR27a and miR142-5p directly target Nrf2 3′ UTR and downregulate expression of Nrf2 transcript. [score:11]
Overexpression of miR144, miR153, miR27a and miR142-5p downregulates Nrf2 protein expression in SH-SY5Y cells. [score:8]
In-silico Prediction of Target miRNAs against Human Nrf2 and Experimental Validation of Nrf2 Downregulation by Forced Expression of miR144, miR153, miR27a and miR142-5p. [score:8]
In general, these miRs (miR144, miR153, miR27a, miR142-5p) when individually present can regulate numerous targets/pathways and the effect of particularly targeting Nrf2 may vary from moderate to high depending on the cellular/stressor setting. [score:6]
miR144, miR153, miR27a and miR142-5p abrogates the interaction and binding of corresponding miRs to human Nrf2 3′ UTR, thus indicating Nrf2 as a direct regulatory target of these miRs. [score:5]
To validate whether the computationally predicted miRNAs could target Nrf2 in neuronal system, we chose human neuroblastoma SH-SY5Y, a neuronal-like subline of SK-N-SH cells and overexpressed with each of these miRs (miR144, miR153, miR27a and miR142-5p) individually. [score:5]
Nrf2 transactivation and ARE -driven NQO1 gene expression were reduced by overexpression of different miRs, miR144, miR153, miR27a and miR142-5p. [score:5]
Overexpression of miR144, miR153, miR27a and miR142-5p reduces GCLC and GSR expression affecting GSH/GSSG ratio and cellular ROS levels. [score:5]
In each case, mutation of miR144 (or) miR153 (or) miR27a (or) miR142-5p binding sites on Nrf2 3′ UTR failed to downregulate the luciferase activity as opposed to those observed in WT type reporter construct (Fig. 5B –5E; compare lane 3 vs lane 4). [score:5]
In-silico based identification of Nrf2 dependent molecular pathway and complex network of disease processes that could be regulated at the intersection of miR144, miR153, miR27a and miR142-5p. [score:4]
miR153, miR27a, miR142-5p and miR144 in regulating Nrf2 expression in SH-SY5Y neuronal cells. [score:4]
0051111.g007 Figure 7 In-silico based identification of Nrf2 dependent molecular pathway and complex network of disease processes that could be regulated at the intersection of miR144, miR153, miR27a and miR142-5p. [score:4]
Nrf2 is a Direct Target of miR144, miR153, miR27a and miR142-5p. [score:4]
Mutating miR144, miR153, miR27a and miR142-5p binding sites in Nrf2 3′ UTR confirms Nrf2 as a direct target of miR144/153/27a/142-5p. [score:4]
To further confirm that Nrf2 3′ UTR regulation by miR144, miR153, miR27a, miR142-5p indeed impact the expression of Nrf2 mRNA, we determined the levels of Nrf2 message in SH-SY5Y cells transfected with and without the aforementioned miRs using quantitative real time PCR for Nrf2. [score:4]
Figure S5 Effect of 10 nM each of combination of miR144, miR153, miR27a and miR142-5p on Nrf2 protein expression. [score:3]
The results of Fig. S5 and S6 suggests that in a given cellular context, when these candidate miRs: miR144, miR153, miR27a and miR142-5p co-exist even at low levels, each would bind to Nrf2 via multiple, distinct binding sites and may perhaps increase the robustness and likelihood of targeting Nrf2 and its associated functions. [score:3]
While all the other target genes which are at the intersection of 4 miRs are represented by independent colored lines (miR144-brown; miR153-red; miR27a-black; miR142-5p-purple). [score:3]
As one to many miR:target relationships are likely, we next analyzed the possible strong candidates including Nrf2 that could be mapped at the intersecting points of miR144, miR153, miR27a and miR142-5p using “mirDIP (microRNA: Data Integration Portal)”. [score:3]
Luciferase reporter constructs containing mutation of miR153, miR27a and miR142-5p target sites of Nrf2 3′ UTR were generated using partial overlapping primer based PCR according to Zheng et al. [25]. [score:3]
Overall, this data suggests that Nrf2 is translationally repressed by miR144, miR153, miR27a, miR142-5p in a specific manner. [score:3]
Thus, to test whether the forced expression of selected individual miRNA candidates (miR144, miR153, miR27a and miR142-5p) have any repressing effect on Nrf2 3′ UTR, we used a reporter construct that was cloned with 428 bp of human Nrf2 3′ UTR downstream of luciferase gene. [score:3]
Ectopic expression of miR153 and miR27a resulted in log (2) 8.5 fold and 8.8 fold increase in levels of these miRs respectively (Fig. S1B; S1C). [score:3]
The results show that individual overexpression of miR144, miR153, miR142-5p effected a ∼42% repression and a maximal repression by about ∼68% was shown by miR27a (Fig. 2A). [score:3]
Thus our study is the first to demonstrate that Nrf2 protein could be subjected to translation repression by miR144/miR153/miR27a/miR142-5p in a Keap1 independent manner in neuronal cellular system. [score:3]
Construction of miR-disease Network (MDN) with Respect to miR144/miR153/miR27a/miR142-5p. [score:3]
It is to be noted that DIANA-mirPath analysis populated NFE2L2 as the principal gene at the intersection of miR144, miR153, miR27a, miR142-5p with a highest –ln(p-value) of 20.79 that is mapped to involve in Prion disease by KEGG pathway (Fig. 7B). [score:3]
Thus, future studies should assess the relative timing and involvement of various closely linked events such as translation repression, mRNA deadenylation and decay in miR144/miR153/miR27a/miR142-5p induced silencing of Nrf2. [score:3]
According to our prediction analysis using TargetScan, we observed evolutionarily conserved binding sites for miR27a, miR142-5p, miR153 between 62–68, 83–90, 98–105 respectively in the human Nrf2 3′ UTR (Fig. 1B). [score:3]
Thus, in view of preserving redox potential that is key to a normal cellular physiology, our results suggest that Nrf2 dependent redox homeostasis could be controlled in this neuronal system by regulation of levels of the following miRs: miR144/miR153/miR27a/miR142-5p. [score:2]
The schematic representation of binding sites and the individual mutants for miR144 (site-1 & site-2), miR153, miR27a and miR142-5p in the human Nrf2 3′ UTR was shown in Fig. 5A and the successful incorporation of mutagenized bases was confirmed by sequencing of the individual mutant constructs. [score:1]
miR144, miR153, miR27a and miR142-5p Represses Nrf2 3′ UTR and Endogenous Nrf2 mRNA. [score:1]
SH-SY5Y cells were transfected with either 40 nM of scramble miRNA or combination of miRs (10 nM each of miR144, miR153, miR27a, miR142-5p) for 48 h. (A) Nrf2 immunoblotting was performed in whole cell protein lysates with anti-GAPDH serving as loading control. [score:1]
Totally 28 genes were computed to be at the intersection of 4 different miRs (hsa-miR144/hsa-miR153/hsa-miR27a/hsa-miR142-5p). [score:1]
Cycling parameters for amplifying mutant miR153 include 30 cycles of 98°C/15 sec, 60°C/15 sec, and 68°C/1 min; followed by extension at 68°C/7 min. [score:1]
Based on these criteria, we narrowed down to a list of 4 different miRs (hsa-miR27a, hsa-miR153, hsa-miR142-5p including the already reported hsa-miR144) (Fig. 1A). [score:1]
miR144/miR153/miR27a/miR142-5p Mediated Repression of Nrf2 is Keap1-independent. [score:1]
Figure S6 Integration analysis of multiple miRNAs (miR144/miR153/miR27a/miR142-5p) to various human pathways by DIANA mirPath. [score:1]
miRNA precursors for hsa-miR144, hsa-miR153, hsa-miR27a, hsa-miR142-5p, hsa-miR21, scramble control miR, siPort™ Amine NeoFX and mirVana miRNA isolation kit were purchased from Ambion (Austin, TX). [score:1]
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8
[+] score: 139
Exogenous expression assays revealed that miR-10b and miR-26a, but not miR-146a, can down-regulate the expression of BRCA1 in both triple -negative MDA-MB-231 and luminal epithelial MCF7 breast cancer-derived cells, whereas miR-153 could down-regulate BRCA1 expression only in MCF7 cells. [score:12]
We validated the expression of these five selected miRNAs by qRT-PCR in the 10 cell lines and found that miR-146a was higher expressed in 3 triple -negative breast cancer cell lines: MDA-MB-231, MDA-MB-436 and SUM1315-BRCA1 (Fig. 1c), that miR-153 was higher expressed in 4 triple -negative breast cancer cell lines: MDA-MB-436, SUM1315MO2, SUM149PT and HCC1937 (Fig. 1d), and that miR-146b-5p, miR-132 and miR-212 were expressed in all 10 cell lines at different levels (Fig. S1) without a significant difference between the triple -negative, luminal or benign cell lines. [score:9]
From the selected miRNAs (listed in Table S4), we chose five miRNAs, i. e., two miRNAs (miR-146a and miR-146b-5p) that were previously found to be over-expressed in breast tumors and to down-regulate BRCA1 expression [18] and three miRNAs (miR-132, miR-212, miR-153) that were most frequently predicted to interact with the 3′-UTR of BRCA1. [score:8]
A p-value < 0.05 is considered significant (between triple -negative and luminal cell lines) miR-146a and miR-153 target the 3′-UTR of BRCA1 BRCA1 gene expression is frequently down-regulated in triple -negative breast cancers. [score:7]
Subsequently, we found that miR-153 can induce BRCA1 down-regulation in MCF7 cells and up-regulation in MDA-MB-231 cells. [score:7]
BRCA1 expression is regulated by miR-10b, miR-26a and miR-153The above expression profiling and in silico analyses allowed us to select 4 miRNAs, miR-10b, miR-26a, miR-146a and miR-153 for further analysis. [score:6]
The results obtained (Fig. 2) indicate that miR-153 can down-regulate the expression of BRCA1 in MCF7 cells. [score:6]
These latter data are consistent with our results in MCF7 cells: although BRCA1 was down-regulated by miR-153, it inhibit proliferation. [score:6]
As shown in Fig. 4 the average expression of miR-153 and miR-10b was found to be significantly lower in triple -negative tumors (p = 0.00045 and p = 0.00038, respectively) than in luminal tumors, while the expression of miR-146a was found to be significantly higher in triple -negative tumors (p = 0.000005). [score:5]
In contrast, we found that in MDA-MB-231 cells miR-153 induced BRCA1 up-regulation. [score:4]
These data are compatible with our finding that BRCA1 up-regulation by miR-153 had no effect on the proliferation of MDA-MB-231 cells. [score:4]
BRCA1 expression is regulated by miR-10b, miR-26a and miR-153. [score:4]
Based on our expression profiling results, four candidate miRNAs (miR-10b, miR-26a, miR-146a and miR-153) were selected as being potentially involved in triple -negative breast cancer development. [score:4]
On the other hand, Zhao et al. found that transient transfection of miR-153 into glioblastoma multiforme stem cells (GBM-SCs) can inhibit their stemness properties, repress their growth potential and induce apoptosis [43]. [score:3]
All experiments were performed in triplicate TCGA was queried for the expression of miR-10b, miR-26a, miR-146a and miR-153 in different primary breast cancer tissues. [score:3]
A total of 519 patients with information on ER, PR and HER2 status were selected to compare the expression profiles of four selected miRNAs (miR-10b, miR-26a, miR-146a and miR-153) in the respective tumors. [score:3]
Next, we tested the effect of miR-153 on the expression of BRCA1. [score:3]
Expression of BRCA1 was determined by qRT-PCR in MDA-MB-231 and MCF7 cells transfected with Tmock (transfection reagent only), miR-146a, anti-miR-146a, miR-153, miR10-b and miR-26a. [score:3]
miR-146a and miR-153 target the 3′-UTR of BRCA1. [score:3]
The efficiency of the miRNA mimics and inhibitors was verified by miRNA quantification using qRT-PCR (Fig. S2), revealing sufficient efficiencies only for miR-10b, miR-26a, miR-146a, anti-miR-146a and miR-153. [score:3]
We conclude that also the function of miR-153 is complex, and identifying targets of miR-153 would be an interesting means to better understand its role in cell proliferation and carcinogenesis-related processes. [score:3]
TCGA data analysis also indicated that the average expression of miR-153 is significantly lower in triple -negative breast cancers. [score:3]
On one hand, Anaya-Ruiz et al. reported that silencing of miR-153 significantly inhibited the growth, reduced the proliferation and induced apoptosis in the triple -negative sporadic breast cancer-derived cell line MDA-MB-231. [score:3]
The above expression profiling and in silico analyses allowed us to select 4 miRNAs, miR-10b, miR-26a, miR-146a and miR-153 for further analysis. [score:3]
Differential expression of miR-10b, miR-26a, miR-146a and miR-153 in TCGA. [score:3]
These results indicate that miR-153 may function as an oncogenic miRNA, whose deregulation could be involved in the initiation and/or development of human breast cancer [41]. [score:3]
Zhao S. Deng Y. Liu Y. Chen X. Yang G. Mu Y. Zhang D. Kang J. Wu Z. MicroRNA-153 is tumor suppressive in glioblastoma stem cellsMol. [score:2]
The expression of four miRNAs (miR-10b, miR-26a, miR-146a and miR-153) was compared in 88 breast tumors with a negative ER, PR and HER2 status (i. e., triple negative phenotype) and in 431 breast tumors that were positive for at least one of the receptors. [score:2]
In MCF7 cells, miR-153, miR-10b and miR-26a significantly inhibited proliferation compared to mock -transfected cells (Fig. 3). [score:2]
Here, expression profiling, transfection and in silico assays were performed to identify potential triple -negative breast cancer miRNA biomarkers, i. e., miR-10b, miR-26a, miR-146a and miR-153. [score:2]
Based on these results we focused our further analyses, next to miR-10b and miR-26a, on miR-146a and miR-153. [score:1]
In another report, Wu et al. suggested that miR-153 may play an important role in promoting the proliferation of human prostate cancer cells and, as such, may represent a novel mechanism of miRNA -mediated PTEN silencing in prostate cancer cells [42]. [score:1]
To assess the effect of miR-10b, miR-26a, miR146a, anti-miR-146a and miR-153 on MDA-MB-231 and MCF7 cell proliferation, the cells were transfected with the respective (anti-) miRNAs, as also siBRCA1 and Tmock (transfection reagent alone). [score:1]
Cells were transfected with Tmock (transfection reagent only), siBRCA1, miR-146a, anti-miR-146, miR-153, miR-10b and miR-26a. [score:1]
This difference in response observed between MDA-MB-231 and MCF7 cells may be explained by differences in the endogenous levels of miR-153, i. e., higher in luminal MCF7 cells and lower in triple -negative MDA-MB-231 cells. [score:1]
MDA-MB-231 cells and MCF7 cells were collected, seeded at a density of 3000 cells per well into a 96-well plate and cultured in a humified incubator at 37 °C containing 5 % CO2 for 24 h. Subsequently, the cells were transfected with Tmock (transfection reagent alone), siBRCA1, miR-146a, anti-miR-146, miR-153, miR-10b and miR-26a using Lipofectamine 2000 reagent (Invitrogen, CA, USA) according to the manufacturer’s protocol. [score:1]
Using bioinformatic tools, we identified a binding site for miR-153 in the 3′-UTR of BRCA1. [score:1]
M. Anaya-Ruiz, J. Cebada, G. Delgado-López, M. L. Sánchez-Vázquez, J. L. M. Pérez-Santos, miR-153 silencing induces apoptosis in the MDA-MB-231 breast cancer cell line. [score:1]
In conclusion, we identified miR-10b, miR-26a, miR-146a and miR-153 as potential triple -negative breast cancer biomarkers. [score:1]
The result of anti-miR-153 is not presented since anti-miR-153 was not effective. [score:1]
[1 to 20 of 40 sentences]
9
[+] score: 127
Other miRNAs from this paper: hsa-mir-200b, hsa-mir-153-1, hsa-mir-200c, hsa-mir-200a, hsa-mir-506
Targeting and inhibition of translation of Snail1 by miR-153, Slug by miR-506 and ZEB1 by miR-200b in HCC cells. [score:7]
Three miRNAs (miR-153, miR-506 and miR-200b) that target 3′-UTR of Snail1, Slug and ZEB1 mRNAs, respectively, were found to be induced by KLF4 overexpression, and suppressed by KLF4 depletion, in HCC cells. [score:7]
For example, miR-200 family has been shown to inhibit ZEB1 and ZEB2 [19– 23], miR-506 has been shown to block Slug translation [24– 27], and miR-153 has been shown to suppress Snail1 and ZEB2 [28]. [score:7]
Targeting inhibition of translation of Snail1 by miR-153, Slug by miR-506 and ZEB1 by miR-200b in HCC cells. [score:7]
The luciferase activities were quantified in these cells, suggesting that miR-153 targets 3′UTR of Snail1 mRNA to inhibit its translation (Figure 2E). [score:7]
Further, miR-506 has been shown to block Slug translation [24– 27], and miR-153 has been shown to suppress Snail1 and ZEB2 [28]. [score:5]
KLF4 may suppress the HCC cell growth and invasion through miR-153, miR-506 and miR-200b -mediated suppression of Snail1, Slug and ZEB1, respectively. [score:5]
Figure 7 KLF4 may suppress the HCC cell growth and invasion through miR-153, miR-506 and miR-200b -mediated suppression of Snail1, Slug and ZEB1, respectively. [score:5]
We found that miR-153, miR-506 and miR-200b depletion abolished the suppressive effects of KLF4 on HCC cell growth (Figure 6A) and invasion (Figure 6B), suggesting that KLF4 may inhibit the HCC cell growth and invasion through miR-153, miR-506 and miR-200b. [score:5]
MiR-153, miR-506 and miR-200b overexpression inhibits HCC cell growth. [score:5]
These data suggest that miR-153, miR-506 and miR-200b overexpression inhibits HCC cell growth. [score:5]
By bioinformatics analyses, we found that miR-153 bound to 3′UTR of Snail1 mRNA at 440-448 base site (A), miR-506 bound to 3′UTR of Slug mRNA at both 439-446 and 843-849 base sites (B), and miR-200b bound to 3′UTR of ZEB1 mRNA at both 463-479 and 892-898 base sites (C) D. We either overexpressed miR-153, miR-506 and miR-200b, or inhibited miR-153, miR-506 and miR-200b in both. [score:5]
MiR-153, miR-506 and miR-200b overexpression suppresses HCC cell invasion. [score:5]
In a loss-of-function experiment, we suppressed the levels of miR-153, miR-506 and miR-200b in KLF4 -overexpressing HCC cells, which completely abolished the effects of KLF4 on cell growth and invasion. [score:5]
These data suggest that miR-153, miR-506 and miR-200b overexpression suppresses HCC cell invasion. [score:5]
In order to confirm that these specific bindings (miR-153/Snail1, miR-506/Slug, miR-200b/ZEB1) are functional, we either overexpressed miR-153, miR-506 and miR-200b, or inhibited miR-153, miR-506 and miR-200b in both. [score:5]
Figure 5In order to confirm that KLF4 may affect the HCC cell growth and invasion through miR-153, miR-506 and miR-200b, we overexpressed the antisense for miR-153, miR-506 and miR-200b in KLF4 -expressing HepG2 cells, and compared to HepG2-KLF4 cells and HepG2-scr cells. [score:4]
In order to confirm that KLF4 may affect the HCC cell growth and invasion through miR-153, miR-506 and miR-200b, we overexpressed the antisense for miR-153, miR-506 and miR-200b in KLF4 -expressing HepG2 cells, and compared to HepG2-KLF4 cells and HepG2-scr cells. [score:4]
Target sequence was inserted into pGL3-Basic vector (Promega, Madison, WI, USA) to obtain pGL3-Snail1-3′UTR, pGL3-Slug-3′UTR or pGL3-ZEB1-3′UTR, which contain the miR-153, miR-506 or miR-200b binding sequence, respectively. [score:3]
Preparation of miR-153, miR-506 and miR-200b overexpressing HepG2 cells. [score:3]
MiR-153, miR-506 and miR-200b depletion abolishes the suppressive effects of KLF4 on HCC cell growth and invasion. [score:3]
Transfection with either KLF4, scr, shKLF4, miR-153, as-miR-153, null, miR-506, as-miR-506, miR-200b, or as-miR-200b -expressing plasmids was performed with Lipofectamine-2000 (Invitrogen). [score:3]
From all the miRNA candidates, we specifically found that KLF4 overexpression increased the levels of miR-153, miR-506 and miR-200b in both, while KLF4 depletion decreased the levels of miR-153, miR-506 and miR-200b in both (Figure 1C). [score:3]
In order to confirm that KLF4 may affect the HCC cell growth and invasion through miR-153, miR-506 and miR-200b, we overexpressed the antisense for miR-153, miR-506 and miR-200b in KLF4 -expressing HepG2 cells (Figure 5A– 5B), and compared to HepG2-KLF4 cells and HepG2-scr cells in both MTT and transwell cell migration assay. [score:3]
Figure 6Depletion of miR-153, miR-506 and miR-200b abolished the effects of KLF4 on HCC cell growth in an. [score:1]
E. The miR-153 -modified HCC cells were then transfected with 1μg of Snail1-3′UTR luciferase-reporter plasmid. [score:1]
The sequences encoding miR-153, antisense (as)-miR-153, miR-506, as-miR-506, miR-200b, or as-miR-200b were similarly cloned into pLVX-ZsGreen1-C1 vector. [score:1]
and C. The levels of miR-153, miR-506 and miR-200b were shown in KLF4-modifed. [score:1]
Then we examined the effects of miR-153, miR-506 and miR-200b on HCC cell growth in an. [score:1]
Depletion of miR-153, miR-506 and miR-200b abolished the effects of KLF4 on HCC cell growth in an. [score:1]
The miR-153 -modified HCC cells were then transfected with 1μg of Snail1-3′UTR luciferase-reporter plasmid. [score:1]
Depletion of miR-153, miR-506 and miR-200b abolishes the effects of KLF4 on HCC cell growth and invasion. [score:1]
By bioinformatics analyses, we found that miR-153 bound to 3′UTR of Snail1 mRNA at 440-448 base site (Figure 2A), miR-506 bound to 3′UTR of Slug mRNA at both 439-446 and 843-849 base sites (Figure 2B), and miR-200b bound to 3′UTR of ZEB1 mRNA at both 463-479 and 892-898 base sites (Figure 2C). [score:1]
The effects of modifications of miR-153, miR-506 and miR-200b on cell growth in an, in both HepG2 cells (A) and Huh7 cells (B) *p<0.05. [score:1]
KLF4 increases levels of miR-153, miR-506 and miR-200b in HCC cells. [score:1]
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10
[+] score: 102
When cells were exposed to 75 mM ethanol for 5 days followed by a withdrawal period for 5 days, the expression of miR-7 and miR-15B was significantly down-regulated, the expression of miR-152 and miR-153 was unchanged and miR-203 was down-regulated to the extent that it could not be detected (Table 1). [score:11]
Chronic exposure of these cells to 75 mM ethanol for five days resulted in a significant up-regulation of the expression of miR-7 and miR-144 and down-regulation of miR-203 and miR-15B with no significant change in the expression of miR-152 or miR-153 (Table 1). [score:11]
Chronic exposure of these cells to 75 mM ethanol for five days resulted in a significant down-regulation of the expression of miR-153 whereas the expression of miR-7, miR-152 and miR-15B was not significantly altered (Table 1). [score:8]
Specifically, miR-203, miR-144, miR-15B and miR-153 are all predicted to target the α1 isoform of the GABA [A] receptor, miR-7 and miR-153 are known to act co-operatively to regulate the expression of α-synuclein and miR-203, miR-144, miR-152, miR-7 and miR-15B are predicted to target isoforms of the 14-3-3 family. [score:8]
The expression of miR-144 was down-regulated to the extent that it could not be detected and the expression of miR-153 was unchanged. [score:8]
Chronic exposure of these cells to 75 mM ethanol for five days resulted in a significant down-regulation of the expression of miR-7, miR-15B and miR-152 with no change in the expression of miR-153. [score:8]
Only one miRNA, miR-153 was down-regulated following chronic treatment and no miRNA showed changes in expression following chronic-intermittent treatment. [score:6]
The expression of miR-153 was up-regulated by ~7 fold following chronic-intermittent treatment and returned to near normal levels once ethanol was removed. [score:6]
Here we measured the expression of six miRNAs—miR-7, miR-153, miR-152, miR-15B, miR-203 and miR-144—which are predicted to target key genes involved in chronic alcoholism and other neurodegenerative disease. [score:5]
We measured the expression of six miRNAs—miR-7, miR-153, miR-152, miR-15B, miR-203 and miR-144—which are predicted to target key genes involved in chronic alcoholism and other neurodegenerative diseases. [score:5]
This is further emphasized by the up-regulation of miR-153 following chronic-intermittent ethanol exposure which occurs only in SH SY5Y cells and not HEK293T or 1321 N1 cells. [score:4]
However, chronic ethanol exposure followed by withdrawal resulted in a significant up-regulation of miR-7, miR-153, miR-152 and miR-15B. [score:4]
Chronic-intermittent exposure resulted in up-regulation of miR-153 and miR-203. [score:4]
We selected six miRNAs—miR-7, miR-152, miR-153, miR-144, miR-203 and miR-15B—which are predicted to target key genes involved in chronic alcoholism including GABA [A] receptors [18], α-synuclein [19], regulators of G protein signaling [20], and the 14-3-3 family of molecular chaperones [21]. [score:4]
The expression of miR-152, miR-144, miR-15B and miR-153 did not change following either chronic-intermittent ethanol exposure or its removal (Table 2). [score:3]
Furthermore, the expression pattern of these four miRNAs was also significantly different between the three cell lines studied (MANOVA, Cell Line × Treatment Group, miR-7, F [2,8] = 9.92 P < 0.0001; miR-153, F [2,8] = 15.35 P < 0.0001; miR-152, F [2,8] = 10.62 P < 0.0001; miR-15B, F [2,8] = 14.58 P < 0.0001). [score:3]
MiR-7, miR-152, miR-153 and miR-15B were expressed in the 1321 N1 cell line whereas miR-144 and miR-203 were below the threshold for reliable detection. [score:3]
We measured the changes in expression of six miRNAs (miR-7, miR-153, miR-152, miR-144, miR-203 and miR-15B) in HEK293T cells, SH SY5Y neuroblastoma and 1321 N1 cells following ethanol treatment. [score:1]
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11
[+] score: 67
MiR-153, miR-181a and miR-324-5p were found down-regulated in brain tumor cells and proposed to function as tumor suppressors [36], [44]– [46]. [score:6]
As we identified an up-regulation of miR-153, miR-181a/a* and miR-324-5p/3p during the conversion of lt-NES cells into neurons, we became interested in whether an overexpression of these miRNAs in lt-NES cells would promote neuronal differentiation. [score:6]
0059011.g003 Figure 3 (A) Quantitative real-time RT-PCR analyses showing relative expression levels of mature miR-153, miR-181a, miR-181a*, miR-324-5p and miR-324-3p in lt-NES cells (I3 cell line) transduced with either LVTHM-ctr (ctr, for endogenous levels) or the respective LVTHM-miRNA overexpressing lentiviral constructs (LVTHM-miR-153, -miR-324-5p/3p, -miR-181a/a*). [score:5]
SYBR Green -based qRT-PCR analyses confirmed that expression levels of miR-153 and miR-324-5p/3p are up-regulated in neural cells compared to hES cells and further increased upon differentiation (Figure 2E, F). [score:5]
Furthermore, miR-181a as well as miR-153 and miR-324-5p were shown to act as tumor suppressors in human brain cancer cells (miR-181a, [44]; miR-324-5p, [36]; miR-153, [45], [46]). [score:3]
MiR-153 was suggested as brain-specific miRNA [33] and found preferentially expressed in neurons [34]. [score:3]
Figure S3 Overexpression of miR-153, miR-181a/a* and miR-324-5p/3p impairs the rate of BrdU incorporation in lt-NES cells. [score:3]
The rate of BrdU incorporation in lt-NES cells under self-renewing culture conditions was significantly reduced by 9.41±2.53%, 22.77±6.03% and 17.73±4,76% upon overexpression of miR-153, miR-181a/a* and miR-324-5p/3p, respectively (Figure 3B and Figure S3). [score:3]
Overexpression of miR-153 and miR-324-5p, however, had no signifcant effect on either TH -positive or GAD -positive neurons (Figure 4C, D). [score:3]
Ectopic expression of miR-153 or miR-181a/a* during differentiation further increased the fraction of β-III tubulin -positive neurons to 7.60±1.58% or 11.59±1.79%, respectively (Figure 3D). [score:3]
Interestingly, miR-153, miR-181a/a* and miR-324-5p/3p are all predicted to target members of the Notch pathway. [score:3]
Ectopic expression of miR-153, miR-181a/a* and miR-324-5p/3p shifts lt-NES cells from self-renewal to neuronal differentiation and promotes neurite outgrowth. [score:3]
Among the miRNAs found up-regulated in lt-NES cells and differentiating neurons compared to hES cells, we selected miR-153, miR-324-5p/3p and miR-181a/a* for further analyses. [score:3]
Overexpression of miR-153, miR-181a/a* or miR-324-5p/3p shifts lt-NES cells from self-renewal to neuronal differentiation. [score:3]
We also observed significantly longer neurites in lt-NES-derived neurons overexpressing miR-153, miR-181a/a* or miR-324-5p/3p, compared to neurons in control cultures (Figure 3E, G). [score:2]
We thus wondered whether the identified neural -associated miRNAs (miR-153, miR-181a/a*, miR-324-5p/3p) could also affect the development of specific neuronal subtypes with a particular focus on the dopaminergic lineage. [score:2]
We validated the expression patterns of miR-181a, miR-181a*, miR-153, miR-324-5p and miR-324-3p both in I3 and in H9.2 cell lines, using Northern blotting and SYBR Green -based qRT-PCR assays (Figure 2D–F). [score:2]
Immunostainings for BrdU in lt-NES cultures (I3 cell line) transduced with LVTHM-ctr and LVTHM-miR-153, -miR-181a/a* and -miR-324-5p/3p constructs. [score:1]
Histogram showing the percentage of TH -positive neurons in untransduced lt-NES cells (I3 cell line, dashed line) and in lt-NES cells transduced with LVTHM-ctr, -miR-124, -miR-125, -miR-153, -miR-181a/a* and miR-324-5p/3p constructs, respectively, after 15 days of differentiation. [score:1]
Among these, we found miR-153, miR-324-5p/3p and the miR-181 family (Figure 1E right panel), for which evidence from other studies points to potential roles in the nervous system. [score:1]
We show that miR-153, miR-324-5p/3p and miR-181a/a* contribute to shifting lt-NES cells from self-renewal to neuronal differentiation. [score:1]
We show that miR-181a/a*, miR-153 and miR-324-5p/3p contribute to the shift from lt-NES cell self-renewal to neuronal differentiation. [score:1]
Taken together our data demonstrate that miR-153, miR-181a/a* and miR-324-5p/3p contribute to the transition of lt-NES cells from self-renewal to neuronal differentiation. [score:1]
In analogy to these observations in a neoplastic background, we found that miR-153 and miR-181a/a* impair proliferation of non-tumorigenic human neural stem cells and promote their neuronal differentiation. [score:1]
Specifically, reintroduction of miR-181a and miR-153 in glioblastoma cells impaired their proliferation [44], [45]. [score:1]
Upon transduction of lt-NES cells with LVTHM-miR-153, LVTHM-miR-181a/a* or LVTHM-miR-324-5p/3p we observed a stable increase of the respective endogenous miRNA levels (Figure 3A). [score:1]
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[+] score: 48
For each approach (I: gene expression, II: combination of gene expression and genome CNA, III: combination of gene expression, genome CNA, and miRNA analysis, IV: genes overlapping with other gene signatures, V: co-expressed gene list, VI: co-rank miRNA list), the Area Under Curve AUC results of normal versus aggressive PC classification are presented in Figure 4. For the VI approach (miRNA signature), we used hsa-miR-153. [score:9]
In the V approach, the co -expression network associated with the identified four genes allowed to place these four genes in a more extended network of 19 co-expressed genes, in which the hsa-miR-153 seems to regulate a significant higher number of target genes (VI approach). [score:8]
Four of the 19 genes (EPHA3, KLF5, EFNA5, and EFNA3) of the described gene co -expression signature are possible targets of hsa-miR-153. [score:5]
Yuan Y. Du W. Wang Y. Xu C. Wang J. Zhang Y. Wang H. Ju J. Zhao L. Wang Z. Suppression of AKT expression by miR-153 produced anti-tumor activity in lung cancerInt. [score:5]
Shan N. Shen L. Wang J. He D. Duan C. MiR-153 inhibits migration and invasion of human non-small-cell lung cancer by targeting ADAM19Biochem. [score:4]
We found one miRNA (hsa-miR-153) that could control a sub-pathway of the co -expression network. [score:3]
Although a biological experimental validation of miRNA silencing and its relation to the expression of the four-gene signature is lacking in this work, our in-silico results show that hsa-miR-153 may represent a single miRNA -based signature potentially suitable to be used in clinical non-invasive tests and at limited costs for a diagnostic purpose and may thus open new therapeutic approaches in PC. [score:3]
In particular, hsa-miR-153 could regulate four genes, namely, EPHA3, KLF5, EFNA5, and EFNA3. [score:2]
Zhao S. Deng Y. Liu Y. Chen X. Yang G. Mu Y. Zhang D. Kang J. Wu Z. MicroRNA-153 is tumor suppressive in glioblastoma stem cellsMol. [score:2]
Although the combination strategy allowed to reduce the number of genes from 3069 to 21 (from I to III), all genes signatures derived by the five approaches (I, II, III, IV, V, VI) achieved good performance, but better results were found for method VI (hsa-miR-153). [score:1]
Analysing the literature, miR-153 has been already isolated in circulating biofluids (i. e., plasma and whole blood) in several pathological conditions, although not related to PC [20, 21, 22]. [score:1]
Anaya-Ruiz M. Cebada J. Delgado-López G. Sánchez-Vázquez M. L. Pérez-Santos J. L. miR-153 silencing induces apoptosis in the MDA-MB-231 breast cancer cell lineAsian Pac. [score:1]
VI miRNA Signature: hsa-miR-153. [score:1]
However, the VI method (with hsa-miR-153) showed a better AUC performance. [score:1]
From this network, we further found one miRNA, hsa-miR-153, highly connected to the gene network. [score:1]
Regarding specifically miR-153, this miRNA has been already isolated in circulating biofluids (i. e., plasma and whole blood) in pathological conditions, although not related to PC [20, 21, 22]. [score:1]
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[+] score: 24
Upregulation of miR-153 promotes cell proliferation via downregulation of the PTEN tumor suppressor gene in human prostate cancer. [score:9]
The expression of miR-153 is also upregulated by hydrogen peroxidase induced oxidative stress (Narasimhan et al., 2014) and nicotine exposure (Tsai et al., 2014). [score:6]
Hydrogen peroxide responsive miR153 targets Nrf2/ARE cytoprotection in paraquat induced dopaminergic neurotoxicity. [score:3]
In a comprehensive miRNA profiling study using a neurosphere mo del of alcohol exposure, Miranda and his colleagues found a reduction in expressions of miR-21, miR-335, miR-9, and miR-153 24 h after exposure (Sathyan et al., 2007). [score:3]
MiR-153 targets the nuclear factor-1 family and protects against teratogenic effects of ethanol exposure in fetal neural stem cells. [score:2]
The miR-153 and miR-21 also similarly control the cellular proliferation (Zhong et al., 2012; Wu et al., 2013). [score:1]
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[+] score: 23
Other miRNAs from this paper: hsa-mir-22, hsa-mir-29a, hsa-mir-153-1, hsa-mir-146a, hsa-mir-206
A) Luciferase constructs expressing the Renilla luciferase gene under the control of the MAPK14/p38 or Tp53inp1 3′ UTRs were co -transfected in HEK293T cells with either an empty plasmid (pcDNA3.1), plasmid expressing a control miR-153 not predicted to target the 3′ UTR or a plasmid expressing miR-22. [score:9]
0054222.g006 Figure 6A) Luciferase constructs expressing the Renilla luciferase gene under the control of the MAPK14/p38 or Tp53inp1 3′ UTRs were co -transfected in HEK293T cells with either an empty plasmid (pcDNA3.1), plasmid expressing a control miR-153 not predicted to target the 3′ UTR or a plasmid expressing miR-22. [score:9]
In order to first confirm the pertinent target predictions, we used 3′ untranslated region (UTR) luciferase assays to show that miR-22 specifically interacts with the 3′ UTRs of the Rcor1, Rgs2 and HDAC4 mRNAs (Figure 1 ), compared to control miRNAs that are not predicted to target these mRNAs (miR-146a served as the control for Rcor1 and HDAC4 whereas miR-153 served as a control for Rgs2 because Rgs2 contains a predicted miR-146a binding site). [score:5]
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[+] score: 20
MicroRNA-153 physiologically inhibits expression of amyloid-β precursor protein in cultured human fetal brain cells and is dysregulated in a subset of Alzheimer disease patients. [score:7]
Figure 1 Predicted miRNA processing pathways – APP translation and amyloid beta generation may potentially be directly regulated by brain-specific miRNA-153 family. [score:5]
The one strand of the miR-153 in the RISC complex (RNA -induced silencing complex) represses APP translation through APP 3′-UTR mRNA cleavage, whereas the other miRNA strand is degraded. [score:3]
Decreasing of miR-153 levels may lead to increased APP expression (Long et al., 2012) and further amyloid beta production. [score:3]
The resulting hairpins pre-miR-153-1 and pre-miR-153-2 are transferred by Exportin-5 to the cytoplasm, were the Dicer-complex generates the mature biologically active miR-153. [score:1]
Primary miRNA-153-1 and miRNA-153-2 transcripts (pri-miR) produced by RNA polymerase II, is then cleaved by the Drosha complex in the nucleus. [score:1]
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[+] score: 20
The results revealed that PQ could inhibit the expression of miR-200a-3p and miR-21, but up-regulated the levels of miR-141-3p and miR-153 in damaged lung tissues; EPCs injection significantly attenuated the PQ induced-up-regulation of miR-141-3p (approximate to 60%), while EPCs had no significant effect on the expression of miR-200a-3p, miR-21 and miR-153 (Fig.   3a). [score:13]
PQ also caused the dysregulated expression of some miRNAs including miR-200a-3p, miR-21, miR-141-3p and miR-153, and only the level of miR-141-3p was influenced by EPCs. [score:4]
a The expressions of miR-200a-3p, miR-21, miR-141-3p and miR-153 in lung tissues were determined using qRT-PCR. [score:3]
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17
[+] score: 18
Other miRNAs from this paper: hsa-mir-153-1
Enrichment in genes putatively regulated by the microRNA miR-153 was observed among upregulated transcripts (13 genes out of 153 in the annotation: ABAT, FAM168B, PPRC1, DVL3, ZMIZ1, MFAPL3, SLC38A1, XYLT1, ARL4A, ADO, FAM168A, PLEKHA3, AUTS2, p = 1.2 × 10 [−2]). [score:5]
Indeed, annotation analysis of overexpressed transcripts identified enrichment in miR-153 target genes in IPF fibroblasts in our study, suggesting reduced activity of this microRNA. [score:5]
miR-153 expression is reduced in the lungs of mice with bleomycin -induced fibrosis, while knockdown of miR-153 potentiates phosphorylation of Mothers against decapentaplegic homolog (SMAD)2/3 and myofibroblastic transformation induced by TGF-β in a human fetal lung fibroblast cell line [38]. [score:4]
Liang C. Li X. Zhang L. Cui D. Quan X. Yang W. The anti-fibrotic effects of microRNA-153 by targeting TGFBR-2 in pulmonary fibrosis Exp. [score:3]
Of interest, previous studies identified miR-153 as a potential endogenous repressor of lung fibrogenesis. [score:1]
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18
[+] score: 17
REST directly down-regulates a large number of genes at the transcriptional level, but also probably indirectly activates the expression of other genes at the post-transcriptional level via the repression of many noncoding targets (Conaco et al., 2006; Mortazavi et al., 2006; Wu and Xie, 2006; Visvanathan et al., 2007; Singh et al., 2008; Johnson et al., 2009), including several micro RNAs (miRNAs) considered to be brain-specific (such as miR9, miR124, miR132, miR135, miR139, and miR153; Figure 1). [score:9]
REST regulates the expression of miRNAs and is itself regulated by them, including miR-153 (Mortazavi et al., 2006; Wu and Xie, 2006), miR-9 and miR-29a (Wu and Xie, 2006; Figure 1). [score:5]
Importantly, REST itself appears to be a predicted target of miR-153 (Mortazavi et al., 2006; Wu and Xie, 2006), miR-9 and miR-29a (Wu and Xie, 2006). [score:3]
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[+] score: 16
For example, miR-181 and miR-153 promote apoptosis by directly targeting B-cell chronic lymphocytic leukemia/lymphoma 2 (Bcl-2) mRNA and repressing its translation, thereby inhibiting gliomagenesis [84]. [score:8]
Xu J. Liao X. Lu N. Liu W. Wong C. W. Chromatin-modifying drugs induce miRNA-153 expression to suppress Irs-2 in glioblastoma cell lines Int. [score:5]
Both miR-181 and miR-153 expression is decreased in glioma cell lines and a subset of clinical glioma specimens, suggesting roles of the two miRNAs in glioma progression. [score:3]
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20
[+] score: 13
miR-107, miR-153 and miR-142-3p indirectly reduce p21 expression through targeting the upstream regulators, FOXO1, PTEN and FOXO4, respectively [50– 52]. [score:7]
For example, miR-107, miR-153, and miR-142-3p had been shown to reduce p21 expression through targeting the upstream regulators, FOXO1, PTEN and FOXO4, respectively [50– 52]. [score:6]
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21
[+] score: 13
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-98, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-107, hsa-mir-16-2, hsa-mir-198, hsa-mir-148a, hsa-mir-30d, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-205, hsa-mir-210, hsa-mir-181a-1, hsa-mir-222, hsa-mir-224, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-27b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-132, hsa-mir-137, hsa-mir-140, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-153-1, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-134, hsa-mir-136, hsa-mir-146a, hsa-mir-150, hsa-mir-184, hsa-mir-185, hsa-mir-186, hsa-mir-206, hsa-mir-320a, hsa-mir-200c, hsa-mir-128-2, hsa-mir-200a, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-299, hsa-mir-26a-2, hsa-mir-373, hsa-mir-376a-1, hsa-mir-342, hsa-mir-133b, hsa-mir-424, hsa-mir-429, hsa-mir-433, hsa-mir-451a, hsa-mir-146b, hsa-mir-494, hsa-mir-193b, hsa-mir-455, hsa-mir-376a-2, hsa-mir-33b, hsa-mir-644a, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-301b, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-320e, hsa-mir-3613, hsa-mir-4668, hsa-mir-4674, hsa-mir-6722
In addition, miR-7 and miR-153 target the 3.0 UTR of SNCA, bind directly to SNCA mRNA to downregulate its expression and are enriched in the brains of PD patients (Doxakis, 2010). [score:9]
Post-transcriptional regulation of alpha synuclein expression by mir-7 and mir-153. [score:4]
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[+] score: 13
This mRNA is targeted by miR-9-5p [47], miR-21-5p, miR-16-5p (TargetScan), miR-183-5p [47], miR-486b-5p [82], and miR-153-3p [47]. [score:5]
miR-195a-5p that has the same seeding sequence with miR-16-5p and is predicted to bind BCL2 mRNA was also downregulated while miR-153-3p that was also found to bind BCL2 experimentally (by Western blot, qRT-PCR, and LUC) [45] was increased. [score:4]
FOXO1 is targeted by a multitude of miRNAs that are changed in our study miR-9-5p, miR-21-5p, miR-16-5p, miR-183-5p [47], miR-486b-5p, and miR-153-3p. [score:3]
miR-153-3p that binds BCL2 experimentally (by WB, qRT-PCR and LUC) [45] was increased in our study and may have the opposite effect, i. e., attenuating the anti-apoptotic effect of the other miRNAs. [score:1]
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23
[+] score: 13
We observed that hsa-miR-153-3p was 13.36 (log FC = 6.68)-fold more abundant in patients with LN class IV than in controls and therefore, through its interaction with the transcription factor fox01, it could be decreasing the expression of hsa-miR-183-5p, which was found to be 6.88 (log FC = 3.44) times less abundant in patients with class LN-IV than in controls, and promoting in the same way an increase in the abundance of miR-145-5p, which we found 6.36(log FC = 3.18) times more in patients with class LN-IV than in controls. [score:3]
The circulating miRNA with the highest relative abundance was miR-153-3p (LogFC of 6.6857) and the miRNA with the lowest relative expression was miR-6741-3p (LogFC of -4.7567) (Table 2) 10.1371/journal. [score:3]
In contrast, eight miRNAs (hsa-miR-153-3p, hsa-miR-6087, hsa-miR-3942-5p, hsa-miR-7977, hsa-miR-323b-3p, hsa-miR-410-3p, hsa-miR-4732-3p and hsa-miR-6741-3p) had no experimentally validated targets described to date. [score:3]
The circulating miRNA with the highest relative abundance was miR-153-3p (LogFC of 6.6857) and the miRNA with the lowest relative expression was miR-6741-3p (LogFC of -4.7567) (Table 2) 10.1371/journal. [score:3]
Alterations in the relative abundance of miR-589-3p, miR-1260b, miR-4511, miR-485-5p, miR-584-5p, miR-543, miR-153-3p, miR-6087, miR-3942-5p, miR-7977, miR-323b-3p, miR-4732-3p and miR-6741-3p, and its possible association with lupus nephritis is described for the first time. [score:1]
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24
[+] score: 11
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26b, hsa-mir-27a, hsa-mir-31, hsa-mir-33a, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-147a, hsa-mir-34a, hsa-mir-182, hsa-mir-199a-2, hsa-mir-212, hsa-mir-221, hsa-mir-224, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-132, hsa-mir-142, hsa-mir-145, hsa-mir-152, hsa-mir-153-1, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-127, hsa-mir-134, hsa-mir-200c, hsa-mir-106b, hsa-mir-361, hsa-mir-148b, hsa-mir-20b, hsa-mir-410, hsa-mir-202, hsa-mir-503, hsa-mir-33b, hsa-mir-643, hsa-mir-659, bta-let-7f-2, bta-mir-103-1, bta-mir-148a, bta-mir-21, bta-mir-221, bta-mir-26b, bta-mir-27a, bta-mir-99a, bta-mir-125a, bta-mir-125b-1, bta-mir-145, bta-mir-199a-1, bta-mir-27b, bta-mir-30b, bta-mir-31, bta-mir-127, bta-mir-142, bta-mir-20b, bta-let-7d, bta-mir-132, bta-mir-148b, bta-mir-200c, bta-mir-22, bta-mir-23a, bta-mir-29b-2, bta-mir-361, bta-let-7g, bta-mir-24-2, bta-let-7a-1, bta-let-7f-1, bta-let-7i, bta-mir-25, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-103-2, bta-mir-125b-2, bta-mir-34a, hsa-mir-708, hsa-mir-147b, hsa-mir-877, hsa-mir-940, hsa-mir-548j, hsa-mir-302e, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-100, bta-mir-106b, bta-mir-130a, bta-mir-134, bta-mir-147, bta-mir-152, bta-mir-153-1, bta-mir-153-2, bta-mir-182, bta-mir-24-1, bta-mir-199a-2, bta-mir-202, bta-mir-212, bta-mir-224, bta-mir-33a, bta-mir-33b, bta-mir-410, bta-mir-708, bta-mir-877, bta-mir-940, bta-mir-29b-1, bta-mir-148c, bta-mir-503, bta-mir-148d
Among the overexpressed miRNAs miR-20b-3p and miR-708-3p showed the highest fold change regulation, while miR-153 and miR-134 exhibit highest fold change among the downregulated miRNAs. [score:7]
In the present study we also found a panel of down regulated miRNAs including miR-153 and miR-134 which are commonly known as tumor suppressor miRNA [52, 53]. [score:4]
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25
[+] score: 10
Based on the collected miRNA-circRNA interactions and the deregulated RNA molecules, we collected several abnormally expressed miRNAs, including 11 downregulated miRNAs (miR-124-3p, miR-129-5p, miR-135a-5p, miR-153-3p, miR-204-5p, miR-208a-3p, miR-211-5p, miR-218-5p, miR-488-3p, miR-490-3p, and miR-504-5p) and 1 upregulated miRNA (miR-373-3p). [score:10]
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26
[+] score: 9
The expression of miR-153 that functions as an oncosuppressor was found to be downregulated in GBM tissues and in cultured CD133+ GSCs. [score:8]
Transfection of miR-153 into these GSCs induced differentiation and apoptosis and stalled tumour growth [64]. [score:1]
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[+] score: 9
Additionally, impairment in miR-64, miR-55, let-7, miR-10a, miR-10b, miR-132, miR-7, miR-153, and miR-435 expressions in symptomatic transgenic PD mice and PD disease mo dels was found to be linked with increased α-syn level [163, 165– 167]. [score:5]
Specifically miR-7 and miR-153 were reported to regulate α-syn expression in worm C. elegans and PD patients brains (Figure 3) [163, 164]. [score:4]
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[+] score: 8
In an in-vitro study using H-69 lung cancer cell line, Pak et al. (2014) reported upregulation of miR-16-2, miR-93, miR-95, mir-153, mir-195, miR-199a-3p, and down-regulation of miR let7a, let7i, miR-124a in the presence of excretory secretory protein of C. sinensis. [score:7]
Among the miRNAs, seven of them (miR-16-2, miR-93, miR-95, miR-136, miR-153, miR-195, and miR-199a-3p) were mainly associated with esophageal adenocarcinoma, breast cancer and colorectal carcinoma, suggesting the role of these miRs in cell-proliferation and cell-signaling. [score:1]
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[+] score: 7
However, only a small number of microRNAs, including miR-28, miR-93, miR-144, miR-153, miR-27a, miR-132, and miR142-5p, have been confirmed experimentally to directly bind to the 3′UTR of Nrf2 and consequently downregulate gene expression [104– 108]. [score:7]
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30
[+] score: 6
Functional studies revealed that miR-153 upregulation increases resistance to Oxaliplatin and Cisplatin in colorectal cancer by inhibiting FOXO3a [81]. [score:6]
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31
[+] score: 6
miR-153, as an independent prognostic marker for predicting survival of gastric cancer patients, is downregulated in GC and promote gastric cancer cell migration and invasion, by inhibiting SNAI1 -induced EMT [18]. [score:6]
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32
[+] score: 6
miR-ID Increased Fold-Changes miR-ID Decreased Fold-Changes miR-29b 8.5 miR-17 15.7 miR-29a 7.7 miR-92a 13.6 miR-29c 7.3 miR-18a 12.0 miR-1224 6.6 miR-192 7.2 miR-133b 2.0 miR-127 2.4 miR-200c 1.7 miR-154 1.9 miR-200a 1.4 miR-21 1.7 miR-205 1.3 miR-680 1.3 miR-208a 1.2 miR-377 1.2 miR-669b 1.2 miR-153 1.1 Figure 3Fucoidan increases the expression of miR-29b. [score:3]
miR-ID Increased Fold-Changes miR-ID Decreased Fold-Changes miR-29b 8.5 miR-17 15.7 miR-29a 7.7 miR-92a 13.6 miR-29c 7.3 miR-18a 12.0 miR-1224 6.6 miR-192 7.2 miR-133b 2.0 miR-127 2.4 miR-200c 1.7 miR-154 1.9 miR-200a 1.4 miR-21 1.7 miR-205 1.3 miR-680 1.3 miR-208a 1.2 miR-377 1.2 miR-669b 1.2 miR-153 1.1 Figure 3Fucoidan increases the expression of miR-29b. [score:3]
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33
[+] score: 6
Other miRNAs from this paper: hsa-mir-200b, hsa-mir-153-1, hsa-mir-200c, hsa-mir-200a, hsa-mir-300
D, E. of Twist protein expression in HN-12 and MDA-MB-231 cells treated with miR-153 mimic (D) or in HN-4 and MCF-7 cells treated with miR-153 inhibitor F, G, H, I. Overexpression of Twist rescued the repressive effects of miR-300 on EMT, leading to morphological changes (F), molecular changes consistent with EMT (G, H), and elevated invasive abilities in transwell assays (I). [score:6]
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34
[+] score: 5
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-96, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, hsa-mir-192, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-211, hsa-mir-212, hsa-mir-181a-1, hsa-mir-214, hsa-mir-217, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-27b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-137, hsa-mir-138-2, hsa-mir-145, hsa-mir-152, hsa-mir-153-1, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-136, hsa-mir-138-1, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-193a, hsa-mir-194-1, hsa-mir-320a, hsa-mir-155, hsa-mir-181b-2, hsa-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-34c, hsa-mir-26a-2, hsa-mir-302b, hsa-mir-369, hsa-mir-375, hsa-mir-378a, hsa-mir-328, hsa-mir-335, hsa-mir-133b, hsa-mir-409, hsa-mir-484, hsa-mir-485, hsa-mir-486-1, hsa-mir-490, hsa-mir-495, hsa-mir-193b, hsa-mir-497, hsa-mir-512-1, hsa-mir-512-2, hsa-mir-506, hsa-mir-509-1, hsa-mir-532, hsa-mir-92b, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-33b, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-1224, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-802, hsa-mir-509-2, hsa-mir-509-3, hsa-mir-548e, hsa-mir-548j, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-548q, hsa-mir-548s, hsa-mir-378b, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-320e, hsa-mir-548x, hsa-mir-378c, hsa-mir-4262, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-378f, hsa-mir-378g, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-378h, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-378i, hsa-mir-548am, hsa-mir-548an, hsa-mir-203b, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-378j, hsa-mir-548ay, hsa-mir-548az, hsa-mir-486-2, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
Ethanol exposure to neurons in culture decreased the expression of miR-9, miR-21, miR-153 and miR-335 [110, 111, 112]. [score:3]
Tsai P. C. Bake S. Balaraman S. Rawlings J. Holgate R. R. Dubois D. Miranda R. C. MiR-153 targets the nuclear factor-1 family and protects against teratogenic effects of ethanol exposure in fetal neural stem cells Biol. [score:2]
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35
[+] score: 5
MiR-153 promotes proliferation of human prostate cancer cells through direct suppression of PTEN expression (97). [score:5]
[1 to 20 of 1 sentences]
36
[+] score: 5
Many semaphorins and their receptors are predicted targets of brain-expressed miRNAs (e. g., let-7c, miR-125b, miR-153, miR-103, miR-323, miR-326, and miR-337). [score:5]
[1 to 20 of 1 sentences]
37
[+] score: 5
Emerging evidence has also supported that multiple miRNAs such as miR-200c [22, 23], miR-153 [24], miR-126 [25, 26], miR-19a [27], miR-32 [28], govern the cell invasion and metastasis in CRC through targeting their specific targets. [score:5]
[1 to 20 of 1 sentences]
38
[+] score: 5
On the other hand, miR-153, -100, -125b, -10a, -99a, -376a, -379, -651, and -146b were significantly lower in expression in the two ESCC cell lines than in Het-1A cells (Figure 1B). [score:3]
On the other hand, miR-153, -100, -125b, -10a, -99a, -376a, -379, -651, and -146b were significantly reduced in expression in both ESCC cell lines compared to Het-1A cells (B). [score:2]
[1 to 20 of 2 sentences]
39
[+] score: 5
Adipose-derived exosomes isolated from serum and urine of obese youths with physician-diagnosed asthma showed differential expression of miRNAs (miR-15a-5p, miR-153-3p, and miR-138-5p) which target TGF-β signaling and is associated with poor asthma outcome (228). [score:5]
[1 to 20 of 1 sentences]
40
[+] score: 4
Post-transcriptional regulation of alpha-synuclein expression by mir-7 and mir-153. [score:4]
[1 to 20 of 1 sentences]
41
[+] score: 4
In contrast, seven of the apoptosis -associated miRNAs, including miR-153, miR-155, miR-182, miR-202, miR-204, miR-296 and miR-337, were obviously down-regulated. [score:4]
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42
[+] score: 4
For example, knockdown of miR-153 caused a sevenfold increase in spontaneous body movement, and the synaptic protein SNAP-25, which is involved in vesicular exocytosis, was found to be the target (97). [score:4]
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43
[+] score: 4
Ectopic expression of miR-153, miR-181a/181a*, and miR-324-5p/3p shifted lt-NES cells from self-renewal to neuronal differentiation. [score:3]
This extensive profiling pointed to additional miRNAs enriched in differentiated neurons, miR-125b, miR-153, miR-181a/181a*, and the cluster miR-324-5p/3p. [score:1]
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44
[+] score: 4
Oncogenic miRNAs like hsa-miR-339-5p, hsa-miR-143-5p, hsa-miR-409-3p, hsa-miR-153-3p and hsa-miR-145-5p have been reported to be downregulated in breast cancer [31– 35]. [score:4]
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45
[+] score: 4
The RNA oligonucleotide probes (Integrated DNA Technologies) used for miRNA enrichment are as follows: miR-36c*: 5′ ACCGUGAGAGACUAUCCCG 3′; miR-71: 5′ UCACUACCCAUGUCUUUCA 3′; miR-153: 5′ CACUUUUGUGACUAUGCAA 3′ and miR-5842*: 5′ UAGCAGGAUGUAUCCAUCG 3′. [score:1]
The RNA oligonucleotide probes (Integrated DNA Technologies) used for miRNA enrichment are as follows:miR-36c*: 5′ ACCGUGAGAGACUAUCCCG 3′;miR-71: 5′ UCACUACCCAUGUCUUUCA 3′;miR-153: 5′ CACUUUUGUGACUAUGCAA 3′ andmiR-5842*: 5′ UAGCAGGAUGUAUCCAUCG 3′. [score:1]
The autoradiographs of the p19 isolated miRNA:RNA probe duplexes show that miR-36c* is preferentially detected in RNA from female parasites, while miR-71, miR-153 and miR-5842* are more abundant in RNA from mf then adults (Figure 2). [score:1]
B. malayi miR-71, miR-36c*, mir-153 and miR-5842* identified in the small RNA libraries were confirmed using the p19 miRNA detection kit (NEB, [43]). [score:1]
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46
[+] score: 4
Liang et al. [30] has reported that miR-153 has anti-fibrotic effect on TGF-β1 -treated pulmonary fibroblasts by down-regulation of TGFBR2. [score:4]
[1 to 20 of 1 sentences]
47
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-96, hsa-mir-99a, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-139, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-210, hsa-mir-181a-1, hsa-mir-214, hsa-mir-215, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-224, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-130a, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-153-1, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-134, hsa-mir-136, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-190a, hsa-mir-194-1, hsa-mir-195, hsa-mir-206, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-101-2, hsa-mir-219a-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-99b, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-370, hsa-mir-373, hsa-mir-374a, hsa-mir-375, hsa-mir-376a-1, hsa-mir-151a, hsa-mir-148b, hsa-mir-331, hsa-mir-338, hsa-mir-335, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-429, hsa-mir-491, hsa-mir-146b, hsa-mir-193b, hsa-mir-181d, hsa-mir-517a, hsa-mir-500a, hsa-mir-376a-2, hsa-mir-92b, hsa-mir-33b, hsa-mir-637, hsa-mir-151b, hsa-mir-298, hsa-mir-190b, hsa-mir-374b, hsa-mir-500b, hsa-mir-374c, hsa-mir-219b, hsa-mir-203b
Ethanol exposure down-regulate miR-21, miR-335, miR-9, and miR-153 (Sathyan et al., 2007). [score:4]
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48
[+] score: 4
For example, the miRNAs miR-21, miR-153, miR-216a, miR-217, miR-494 and miR-10a-5p have been shown to be upregulated in sorafenib-resistant cells and to participate in the mechanisms that are underlying sorafenib resistance [193]. [score:4]
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49
[+] score: 3
Only five miRNAs were intronic in genes that play a role in the mRNA subtype classification (hsa-mir-324 in ACADVL, hsa-mir-153 in PTPRN2, hsa-mir-934 in VGLL1, hsa-mir-595 in PTPRN2, hsa-mir-744 in MAP2K4), demonstrating that the miRNA differential expression is not merely a recapitulation of the mRNA classification. [score:3]
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50
[+] score: 3
Other miRNAs from this paper: hsa-mir-34a, hsa-mir-153-1
A report indicates that microRNA-153 promotes Wnt/β-catenin activation in hepatocellular carcinoma through the suppression of WWOX. [score:3]
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51
[+] score: 3
Several research reported that PTEN function as a target gene of miR-21 [28], miR-214 [29], miR-494 [30], miR-26a [31], miR-144 [32] and miR-153 [33]. [score:3]
[1 to 20 of 1 sentences]
52
[+] score: 3
As α-synuclein inclusions is the major component of Lewy body, miRNAs (miR-34b, miR-34c, miR-153 and miR-7) could target 3’UTR of α-synuclein and ameliorate its toxic effects [53, 54]. [score:3]
[1 to 20 of 1 sentences]
53
[+] score: 3
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-100, hsa-mir-101-1, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-34a, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-30b, hsa-mir-144, hsa-mir-153-1, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-1-1, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-30e, hsa-mir-92b, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-769, hsa-mir-548e, hsa-mir-548j, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-548q, bma-let-7, bma-lin-4, bma-mir-2a, bma-mir-2b-1, bma-mir-2b-2, bma-mir-2c, bma-mir-9, bma-mir-34, bma-mir-71, bma-mir-72, bma-mir-92, bma-mir-100a, bma-mir-100b, bma-mir-100c, bma-mir-100d, bma-mir-153, bma-mir-228, bma-mir-279, hsa-mir-548s, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-548x, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-548am, hsa-mir-548an, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-548ay, hsa-mir-548az, bma-mir-2i, bma-mir-2g, bma-mir-2e, hsa-mir-548ba, bma-mir-252, bma-mir-2d, bma-mir-84-1, bma-mir-84-2, bma-mir-2f, bma-mir-2h-1, bma-mir-2h-2, hsa-mir-548bb, hsa-mir-548bc
Interestingly, we also found several miRNA* in our dataset with much higher expression levels than their mature partners, such as dim-miR-153* (immature/mature sequence read ratio: ~2/1), dim-miR-1422i* (~39/1), dim-miR-144* (~9/1), miR-200a* (~42/1), miR-9b* (~118/1). [score:3]
[1 to 20 of 1 sentences]
54
[+] score: 3
In neural stem cells, NFIA inhibition by miR-153 repressed early gliogenesis [32]. [score:3]
[1 to 20 of 1 sentences]
55
[+] score: 3
Other miRNAs from this paper: hsa-mir-34a, hsa-mir-153-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-335
Hydrogen peroxide responsive miR153 targets Nrf2/ARE cytoprotection in paraquat induced dopaminergic neurotoxicity. [score:3]
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56
[+] score: 3
Other miRNAs from this paper: hsa-mir-27a, hsa-mir-27b, hsa-mir-142, hsa-mir-144, hsa-mir-153-1
Narasimhan M et al. obtained evidence that the Nrf2 mRNA abundance and nucleo-cytoplasmic concentration of Nrf2 could be directly regulated by miR153/miR27a/miR142-5p/miR144 in a Keap1-independent manner in SH-SY5Y dopaminergic neurons [41, 42]. [score:3]
[1 to 20 of 1 sentences]
57
[+] score: 3
MiR-153 is a novel regulator of EMT that targets ZEB2 and SNAI1 [64]. [score:3]
[1 to 20 of 1 sentences]
58
[+] score: 2
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-101-1, hsa-mir-106a, hsa-mir-107, hsa-mir-16-2, hsa-mir-192, hsa-mir-196a-1, hsa-mir-199a-1, hsa-mir-129-1, hsa-mir-148a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-203a, hsa-mir-210, hsa-mir-212, hsa-mir-214, hsa-mir-215, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-27b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-153-1, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-129-2, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-195, hsa-mir-206, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-181b-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-200a, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-130b, hsa-mir-376c, hsa-mir-375, hsa-mir-378a, hsa-mir-148b, hsa-mir-338, hsa-mir-335, hsa-mir-423, hsa-mir-20b, hsa-mir-429, hsa-mir-449a, hsa-mir-433, hsa-mir-451a, hsa-mir-193b, hsa-mir-520d, hsa-mir-503, hsa-mir-92b, hsa-mir-610, hsa-mir-630, hsa-mir-650, hsa-mir-449b, hsa-mir-421, hsa-mir-449c, hsa-mir-378d-2, hsa-mir-744, hsa-mir-1207, hsa-mir-1266, hsa-mir-378b, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-4512, hsa-mir-378i, hsa-mir-203b, hsa-mir-451b, hsa-mir-378j
Zhang Z. Sun J. Bai Z. Li H. He S. Chen R. Che X. MicroRNA-153 acts as a prognostic marker in gastric cancer and its role in cell migration and invasion OncoTargets Ther. [score:2]
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59
[+] score: 2
Briefly, miRNA was reverse transcribed using sequence specific stem-loop primers (invitrogen) to the following miRNAs: hsa-miR-125b, hsa-miR-145, hsa-miR-153, hsa-miR-210, hsa-miR-143, hsa-miR-100, hsa-miR-363, hsa-miR-451, hsa-miR-572 and hsa-miR-508-5p, based on microarray analysis and their predicted target genes. [score:2]
[1 to 20 of 1 sentences]
60
[+] score: 2
Similarly, Doxakis showed that the combination of miR-7 and miR-153 resulted in a greater reduction in the expression of α-synuclein, the major component of pathological Lewy bodies in the brain, compared to either miRNA alone [19]. [score:2]
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61
[+] score: 2
Among the non-conserved clusters, we identified a cluster with two cat-specific miRNAs on chromosome X (mir-chrX_38640 and mir-chrX_38642), a cluster containing miR-153 and a cat-specific miRNA on chromosome A2, and a cluster on chromosome E2 containing mir-295, mir-302d-1 and mir-371. [score:1]
Among them, miR-219, miR-124, miR-153, miR-128, miR-132 and miR-139 are known to be brain enriched or brain-specific in other species and to be involved in several brain-specific functions [28]. [score:1]
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62
[+] score: 2
The results of miRror2.0 for the input of mmu miR-98, mmu miR-124, mmu miR-153 and mmu miR-361 are shown. [score:1]
Figure 2A shows the difference in the mapping of the four selected mouse miRNAs (mmu-miR-124, mmu-miR-153, mmu-miR-361 and mmu-miR-98; only four miRNAs were selected for simplicity). [score:1]
[1 to 20 of 2 sentences]
63
[+] score: 1
Interestingly, miR-153-2 is within intron 19 of PTRN2, but we were unable to detect this microRNA in our neutrophil samples. [score:1]
[1 to 20 of 1 sentences]
64
[+] score: 1
A0: miR-21 in NTT; A1: miR-21 in TT; B0: miR-145 in NTT; B1: miR-145 in TT; C0: miR-153 in NTT; C1: miR-153 in TT. [score:1]
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Fkih Mhamed I. Privat M. Ponelle F. Penault-Llorca F. Kenani A. Bignon Y. J. Identification of miR-10b, miR-26a, miR-146a and miR-153 as potential triple -negative breast cancer biomarkers Cell. [score:1]
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66
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Other miRNAs from this paper: hsa-mir-153-1
An example with hsa-miR-153 entered in the name field is shown in Figure 4a, while the output is shown in Figure 4b. [score:1]
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67
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Identification of miR-10b, miR-26a, miR-146a and miR-153 as potential triple -negative breast cancer biomarkers. [score:1]
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[2]miR-153-3p is identical to mammalian miR-153-3p from nucleotides 1–21. [score:1]
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69
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Other miRNAs from this paper: hsa-mir-153-1
Rice ears were harvested at least 40 days after heading and dried in a ventilated incubator (MIR-153, Panasonic Healthcare Co. ) [score:1]
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