sort by

48 publications mentioning hsa-mir-452

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-452. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 267
In our study, we revealed these following novel findings: (i) Serial passages of the spheres with doxorubicin and sorafenib could enrich CSC populations in vitro; (ii) miR-452 was identified to promote stem-like properties of HCC; (iii) Sox7 was a direct and functionally relevant target of miR-452 in HCC; (iv) Combination of doxorubicin and ATRA efficiently suppressed metastasis formation of miR-452 overexpressed HCC. [score:8]
For miR-452 up-regulation and down-regulation, LM3 and Huh-7 cells were labeled with luciferase using a lentiviral -based approach. [score:7]
Intriguingly, miR-452 was down-regulated in gliomas [12], breast cancer [13], while its expression increased in HCC [14], clear cell renal cell carcinoma [15], esophageal cancer [16], urothelial carcinoma [17] and prostate cancer stem cells [18]. [score:6]
In our study, we found that the mRNA of β-catenin was significantly elevated when miR-452 was overexpressed (Supplementary Table S2), and markedly declined when miR-452 was down-regulated (Supplementary Table S4). [score:6]
The expressions of SOX7 were drastically (C) decreased upon miR-452 overexpressed, and (D) increased after miR-452 knockdown in both LM3 and Huh7. [score:6]
In our study, Sox7 was confirmed to be a direct target of miR-452 and its low expression indicated poor survival of HCC patients. [score:6]
Combination of doxorubicin and ATRA chemotherapy efficiently suppressed metastasis of miR-452 overexpressed HCC. [score:5]
The expression of SOX7 was significantly correlated reciprocally with miR-452 expression (Supplementary Table S1). [score:5]
Definitely, these aforementioned results confirmed that miR-452 promoted tumor initiation, stemness and metastasis by targeting SOX7 expression in HCC. [score:5]
These findings indicated that miR-452 might suppress SOX7 expression through the miR-452 binding sequence in 3′UTR of Sox7. [score:5]
First, we restored SOX7 expression in miR-452 overexpressed clones of LM3 and Huh7 cells by transfection with lenti-SOX7-ORF, termed LM3/miR-452-SOX7 and Huh7/miR-452-SOX7 (Supplementary Figure S5A, S5B). [score:5]
MiR-452 mimic, miR-452 inhibitor, mimic control and inhibitor control were from Qiagen (Germany). [score:5]
Further, the expressions of SOX7 were drastically decreased in both LM3/miR-452 and Huh7/miR-452 cells (Figure 4C), while the expressions of SOX7 were reversed in LM3/ASO-miR-452 and Huh7/ASO-miR-452 cells (Figure 4D). [score:5]
The restoration of SOX7 significantly inhibited migratory and invasive abilities over those of miR-452 overexpressed cells (Figure 5C, 5D). [score:5]
Then, the mRNA expression of these genes were detected by qPCR after transfection of miR-452 mimics or inhibitor into HCC cell lines (data not shown). [score:5]
To further explore the mechanism by which miR-452 exerted its function, more than 300 genes were predicted to be potential targets using publicly available algorithms (TargetScan, miRanda, PicTar). [score:5]
Combination of doxorubicin and ATRA chemotherapy could efficiently suppress metastasis of miR-452 overexpressed HCC. [score:5]
These patients were classified into high or low expression group according to the mean value of miR-452 expression score. [score:5]
First, we found that miR-452 knockdown decreased the expression of stemness-related gene profile (Supplementary Table S4). [score:4]
Figure 2(A) The percentage of CD44+ and CD133+ cells markedly increased upon miR-452 up-regulation both in LM3 and Huh7. [score:4]
Hepatospheres with (B) higher capability of tumorigenicity, (C) higher expression of stemness-related genes, and (D) markedly overexpression of miR-452 compared with the differentiated clones. [score:4]
Moreover, miR-452 down-regulation weakened the self-renewal ability of HCC cells presented with smaller size and less hepatospheres (Figure 3B). [score:4]
Sox7 was a direct and functional target of miR-452 in HCC. [score:4]
The migration and invasion efficiencies were also inhibited after miR-452 knockdown (Supplementary Figure S3B, Figure 3E). [score:4]
Up-regulation of miR-452 in HCC. [score:4]
In our study, we found that miR-452 was up-regulated and predicted poor patient survival and advanced TNM stage in HCC patients. [score:4]
Our previous data obtained by Illumina Solexa sequencing suggested that miR-452 was obviously up-regulated in HCC tissues comparing with their adjacent normal tissues (data not shown). [score:4]
In vivo metastasis assay showed that the combination of doxorubicin and ATRA could significantly inhibit miR-452 overexpressed LM3 metastasis. [score:4]
Down-regulation of miR-452 in HCC. [score:4]
The goal of our study was to explore the molecular mechanisms related to the miR-452 over -expression in regulating CSCs in HCC. [score:4]
Considering the reported biological function of miR-452, we then demonstrated that miR-452 was also markedly overexpressed in chemo-resistant hepatospheres in comparison with the differentiated HepG2 cells by qPCR (Figure 1D). [score:3]
MiR-452 up-regulation in HCC indicated poor patient prognosis. [score:3]
In our study, we also explored the combined treatment of doxorubicin and ATRA in miR-452 overexpressed HCC. [score:3]
Kaplan Meier curves showed that miR-452 overexpression was also associated with poor overall survival of both cohorts (p < 0.001; p < 0.001; Figure 1F). [score:3]
Moreover, high miR-452 expression was positively correlated with poor patient survival (p = 0.002; p = 0.020; Table 1) and advanced TNM stages (p = 0.019; p = 0.023; Figure 1E; Supplementary Table S1) in both cohorts. [score:3]
Re -expression of SOX7 completely or partially, but significantly, eliminated the effects of miR-452 in capabilities of (A) Chemoresistance, (B) Self-renewal, (C) Migration and (D) Invasion in vitro. [score:3]
Notably, miR-452 levels in training cohort were inversely correlated with the expressions of SOX7. [score:3]
The expression of SOX7 was scored in the same way as mentioned in the miR-452 in situ hybridization. [score:3]
Moreover, the expression of nuclear β-catenin was subverted after the restoration of SOX7 in LM3/miR-452 and Huh7/miR-452 cells (Supplementary Figure S6E, S6F). [score:3]
Meanwhile, miR-452 overexpression prompted not only primary (1 [°]) but also secondary (2 [°]) LM3/miR-452 HCC growth (Figure 2E). [score:3]
Next, the nuclear β-catenin was obviously elevated when miR-452 was overexpressed (Figure 6D, Supplementary Figure S6C). [score:3]
In our study, we demonstrated that miR-452 could markedly promote the stemness of HCC cells including the abilities of chemo-resistance, self-renewal and metastasis by targeting Sox7 involving Wnt/β-catenin signaling pathway. [score:3]
Figure 4(A) The sequence of predicted miR-452 binding site and the wild-type (wt- Sox7) or mutant (mut- Sox7) putative target site in the 3′-UTR of Sox7 mRNA sequence. [score:3]
Figure 5Re -expression of SOX7 completely or partially, but significantly, eliminated the effects of miR-452 in capabilities of (A) Chemoresistance, (B) Self-renewal, (C) Migration and (D) Invasion in vitro. [score:3]
While the nuclear β-catenin came to the opposite, when miR-452 was inhibited (Figure 6E, Supplementary Figure S6D). [score:3]
Then, we found that miR-452 promoted a profile of stemness-related genes expression (Supplementary Table S2). [score:3]
More, miR-452 was identified to promote CSCs by inhibiting Sox7 through activating Wnt/β-Catenin Signaling Pathway (Figure 6F). [score:3]
The sequence of the predicted miR-452 binding site and the wild-type (wt- Sox7) or mutant (mut- Sox7) putative target site in the 3′UTR of Sox7 mRNA sequence were shown in Figure 4A. [score:3]
The self-renewal capability of (C) CD44+ and (D) CD133+ cells sorted from LM3, Huh7 and patient#1 were significantly attenuated by miR-452 inhibitor. [score:3]
Taken together, our study demonstrated that miR-452 promoted stem-like traits of HCC, which might be a potential therapeutic target for HCC. [score:3]
Altogether, miR-452 was identified to be targeted Sox7 gene activating Wnt/β-catenin signaling pathway leading to the enhancement of stem-like traits of HCC (Figure 6F). [score:3]
We also identified that miR-452 inhibitor significantly attenuated the self-renewal capability of CD44+ and CD133+ cells sorted from LM3, Huh7 and patient#1 (Figure 3C, 3D). [score:3]
miR-452 targeted SOX7 involving Wnt/β-catenin signaling pathway. [score:3]
Eventually, the tumor incidence was also significantly lower upon miR-452 inhibition (Figure 3F, Supplementary Table S5). [score:3]
For the restoration of SOX7 expression, Lenti-SOX7-ORF and its control were used to transfect LM3/miR-452 and Huh7/miR-452 cells. [score:3]
Restoration of SOX7 expression inhibited miR-452 correlated stem-like characteristics of HCC cells. [score:3]
Then, miR-452 was also overexpressed in HCC tissues than adjacent normal tissues both in training cohort and validation cohort by ISH (Supplementary Figure S1C). [score:3]
The representative immunostaining results of SOX7 were presented in Supplementary Figure S4B, which evidently showed the inverse correlation with miR-452 expression in the same patient (Supplementary Figure S1D). [score:3]
MiR-452 targeted Sox7 by involving Wnt/β-catenin signaling pathway. [score:2]
Further, we also established two miR-452 knockdown stable cell lines (HCC-LM3/ASO-miR-452, Huh7/ASO-miR-452) and their corresponding negative controls (HCC-LM3/ASO-NC, Huh7/ASO-NC) and validated the efficiency (Supplementary Figure S3A). [score:2]
However, in gliomas miR-452 was down-regulated and resulted in the promotion of stem-like characteristics and tumorigenesis [12], which was opposite to these results in HCC. [score:2]
Then, miR-452 knockdown cells were much more sensitive to either doxorubicin or sorafenib (Figure 3A). [score:2]
After all, the potential mechanisms for the differences of miR-452 in regulating CSCs in different malignancies needs to be further studied. [score:2]
The dual-luciferase reporter assays in HEK293T cells revealed that miR-452 overexpression significantly attenuated the activities of luciferase reporters linked to the 3′UTR of Sox7, but failed to reduce the luciferase activities of the mutated 3′UTR (Figure 4B). [score:2]
MiR-452 was overexpressed in HCC cells accumulated by serial passages of hepatospheres combined with chemotherapy in vitro. [score:2]
MiR-452 was overexpressed in HCC cells accumulated by serial passages of hepatospheres combined with chemotherapy in vitroAccording to the distinct hallmarks of stem/progenitor cells such as self-renewal and chemoresistance, we enriched the liver CSCs of HepG2 upon 20 serial passages in serum-free medium combined with 2 mg/mL of doxorubicin and 5 μmol/L sorafenib (Figure 1A). [score:2]
The tumorigenic ability of LM3/miR-452-SOX7 cells was obviously decreased in accordance with the lower tumor incidence (Supplementary Table S6) and smaller tumor size (Figure 5E). [score:1]
LM3/miR-452, Huh7/miR-452 were much more chemo-resistant than LM3/NC, Huh7/NC cells treated with either 2 mg/ml doxorubicin or 5 μM sorafenib (Figure 2B). [score:1]
Figure 3(A) MiR-452 knockdown evidently sensitized LM3 and Huh7 to the chemotherapeutics (** P < 0.001, respectively, t test). [score:1]
Notably, miR-452 also efficiently promoted the migration (Supplementary Figure S2E) and invasion (Figure 2D) of HCC cells in vitro. [score:1]
Restoration of SOX7 inhibited miR-452 mediated stem-like characteristics of HCC. [score:1]
We first found that miR-452 was significantly increased in HCC cell lines comparing with that in L02 (Supplementary Figure S1B). [score:1]
HEK293T cells seeded in 24-well plates were co -transfected with 50 nM of either miR-452 mimic or NC and 100 ng either wild-type or mutant-type 3′UTR of Sox7 firefly luciferase reporter plasmid. [score:1]
First, FACS analysis showed that the proportion of CD44+ and CD133+ subpopulations were significantly elevated in both LM3/miR-452 and Huh7/miR-452 groups (Figure 2A), but not in CD90+ and EpCAM+ subpopulation (Supplementary Figure S2B, 2C). [score:1]
Meanwhile, the restoration of SOX7 could also markedly erase the miR-452 -mediated competence of (E) tumorigenicity in the xenograft mo dels and (F) metastasis formation in vivo metastasis mo dels. [score:1]
We also identified that miR-452 promoted HCC with higher capacities in chemo-resistance, self-renewal, tumorigenicity and metastasis in vitro and in vivo, which was consistent with the study of Zheng Q et al [14]. [score:1]
In vivo xenograft mo del, as few as 1000 LM3/miR-452 cells were enough for tumorigenesis (Supplementary Table S3). [score:1]
LM3/miR-452-SOX7 and Huh7/miR-452-SOX7 HCC cells showed a decreased chemo-resistance to doxorubicin and sorafinib (Figure 5A). [score:1]
MiR-452 antisense oligonucleotides (ASO-miR-452) was inserted into GV280 vector. [score:1]
Tissue staining of miR-452 was scored independently by two pathologists blinded to the clinical data, by multiplication of immunostaining intensity (0–2), and the percentage of immunoreactive cells (0%–100%) resulted in an score ranging from 0 to 2 for each tumor or non-tumor specimens. [score:1]
Apoptosis of (A) LM3/miR-452 and (B) HuH7/miR-452 cells receiving the indicated treatments was assessed by Annexin V-APC staining. [score:1]
Figure 7Apoptosis of (A) LM3/miR-452 and (B) HuH7/miR-452 cells receiving the indicated treatments was assessed by Annexin V-APC staining. [score:1]
5′-DIG and 3′-DIG labeled locked nucleic acid (LNA) modified probes for endogenous miR-452 (Exiqon, Denmark), positive control (U6) and negative control (scramble-miR) were used. [score:1]
The tumor incidence of LM3/miR-452 group was also significantly higher (Supplementary Table S3). [score:1]
Moreover, miR-452 was also markedly increased in CD44+ and CD133+ cells than that in CD44– and CD133– cells sorted from LM3 and Huh7 by MACS (Supplementary Figure S2D). [score:1]
The miR-452 sequence was amplified and inserted into GV254 vector. [score:1]
[1 to 20 of 86 sentences]
2
[+] score: 210
Fig. 4 miR-452 overexpression in MG-63 cells led to the downregulation of BMI1 protein levels miR-452 expression was detected by using quantitative real-time PCR (qRT-PCR) and normalized to U6. [score:8]
miR-452 overexpression in MG-63 cells suppressed cell proliferation, promoted cell apoptosis, inhibited cell invasion, and led to decreased BMI1 protein levels. [score:7]
miR-452 overexpression in MG-63 cells suppressed cell proliferation, promoted cell apoptosis, and inhibited cell invasion in vitro. [score:7]
miR-452 expression was significantly downregulated in osteosarcoma tissues than those in corresponding noncancerous bone tissues (P < 0.001). [score:6]
These findings suggest that miR-452 downregulation may be involved in osteosarcoma formation and progression and that miR-452 would serve as a novel prognostic biomarker for patients with this disease. [score:6]
The results showed that miR-452 overexpression in MG-63 cells led to the downregulation of BMI1 protein levels (Fig.   4). [score:6]
Fig. 4 miR-452 overexpression in MG-63 cells led to the downregulation of BMI1 protein levels Up to now, the exact mechanisms underlying osteosarcoma are not fully understood. [score:6]
Zhang et al. revealed that upregulated miR-452 -suppressed NSCLC cell epithelial-mesenchymal transition and further disrupted migration and invasion [28]. [score:6]
miR-452 could downregulate BMI1 expression in MG-63 cells. [score:6]
miR-452 levels were calculated by the 2 [−ΔCt] method and normalized to U6 small nuclear RNA The median miR-452 expression level was used as a cut-off value to divide all 95 patients into two groups: high miR-452 expression group (n = 48) and low miR-452 expression group (n = 47). [score:5]
As shown in Fig.   2, patients in high miR-452 expression group had longer overall survival than those in low miR-452 expression group (P < 0.001). [score:5]
In the present study, we revealed that the expression of miR-452 was significantly reduced in osteosarcoma tissues, and reduced miR-452 expression was significantly associated with larger tumor size, high tumor grade, advanced clinical stage, and distant metastasis. [score:5]
Zhang Y, Han L, Pang J, Wang Y, Feng F, Jiang Q. Expression of microRNA-452 via adenoviral vector inhibits non-small cell lung cancer cells proliferation and metastasis. [score:5]
He et al. identified BMI1 as a direct target of miR-452 in NSCLC [22]. [score:4]
Thus, loss of miR-452 expression might be involved in osteosarcoma development and serve as a novel biomarker for poor prognosis. [score:4]
d Upregulation of miR-452 impeded cell invasion in MG-63 cells. [score:4]
He et al. showed miR-452 downregulation in NSCLC tissues and its association with positive tumor metastasis and advanced TNM stage [22]. [score:4]
In summary, our research showed miR-452 downregulation in osteosarcoma and its correlation with aggressive clinicopathological features. [score:4]
Decreased miR-452 expression was linked to larger tumor size, high tumor grade, advanced clinical stage, distant metastasis, and shorter overall survival. [score:3]
Therefore, in the current study, we examined miR-452 expression in osteosarcoma specimens and paired adjacent nontumorous tissues and investigated the correlation between miR-452 expression and clinicopathological factors as well as patient’s survival. [score:3]
Fig. 1The relative expression levels of miR-452 in osteosarcoma specimens and matched adjacent noncancerous bone tissues. [score:3]
b miR-452 expression was significantly lower in osteosarcoma specimens than in the corresponding adjacent noncancerous bone tissues. [score:3]
Recently, aberrant miR-452 expression has been demonstrated in glioma [21], non-small cell lung cancer (NSCLC) [22], bladder cancer [23], prostate cancer [24], urothelial carcinoma [25], and hepatocellular carcinoma [26]. [score:3]
Our study also observed decreased BMI1 protein levels in MG-63 cells after miR-452 overexpression. [score:3]
Association between miR-452 expression and clinicopathological factors. [score:3]
As shown in Table  1, we found that low miR-452 expression was significantly associated with larger tumor size (P = 0.012), high tumor grade (P = 0.008), advanced Enneking stage (P < 0.001), and distant metastasis (P = 0.001). [score:3]
Flow cytometry confirmed promoted apoptosis in miR-452-overexpression MG-63 cells (Fig.   3c). [score:3]
In human gliomas, decreased miR-452 expression was correlated with shorter patient survival time [21]. [score:3]
Overexpression of miR-452 in HepG2 and QGY-7703 hepatocellular carcinoma cells dramatically accelerated proliferation, induced cell cycle from G1 to S transition, blocked apoptosis, and promoted cell migration and invasion in vitro [26]. [score:3]
Ectopic expression of miR-452 reduced tumorigenicity in a nude mouse xenograft mo del. [score:3]
Furthermore, overexpression of miR-452 in MCF-7 breast cancer cells could significantly enhance cell apoptotic and increase chemosensitivity to Adriamycin [29]. [score:3]
miR-452 expression was detected by using quantitative real-time PCR (qRT-PCR) and normalized to U6. [score:3]
In these malignancies, miR-452 acts as a potential oncogene or a candidate tumor suppressor in different cellular contexts. [score:3]
Multivariate Cox regression analysis confirmed that low level of miR-452 expression predicted poor prognosis independently. [score:3]
Multivariate analyses using the Cox proportional hazards regression mo del revealed that miR-452 expression (relative risk (RR) 3.263; P = 0.018), tumor grade (RR 3.013; P = 0.022), distant metastasis (RR 4.985; P = 0.003), and Enneking grade (RR 5.458; P = 0.001) were independent prognostic factors for overall survival of osteosarcoma. [score:3]
Decreased miR-452 expression in osteosarcoma samples. [score:3]
a qRT-PCR analysis confirmed increased miR-452 expression in MG-63 cells after miR-452 mimics transfection. [score:3]
However, very little is known about the expression and clinical significance of miR-452 in human osteosarcoma till now. [score:3]
However, there were no significance between miR-452 expression and other clinicopathological factors, such as age, gender, anatomic location, and histological type. [score:3]
Quantitative PCR was conducted at 95 °C for 10 min followed by 40 cycles of 95 °C for 15 s and 60 °C for 60 s. All reactions were run in triplicate, and miR-452 expression was normalized to U6 small nuclear RNA. [score:3]
Decreased miR-452 expression might be an independent biomarker for poor prognosis. [score:3]
For example, Kristensen et al. reported that miR-452 inhibited proliferation, migration, and invasion of PC3 and DU145 prostate cancer cells [24]. [score:3]
Thus, the function of miR-452 may be complex in different cancer types, and the role of miR-452 should be tumor specific and possibly dependent on the nature of its targets. [score:3]
Increased miR-452 expression in bladder urothelial carcinomas was associated with high incidence of lymph nodes metastasis and poor prognosis [25]. [score:3]
Previous research has demonstrated the tumor-suppressive function of miR-452 in several human malignancies. [score:3]
Figure  1a shows decreased miR-452 expression in osteosarcoma compared to matched adjacent noncancerous bone tissues. [score:2]
We also explored the role of miR-452 in the regulation of biological behaviors of osteosarcoma cells. [score:2]
The expression of miR-452 was detected in 95 pairs of osteosarcoma specimens and adjacent noncancerous bone tissues using quantitative RT-PCR (qRT-PCR) assay. [score:2]
MicroRNA-452 (miR-452) was previously reported to be dysregulated in several types of human cancers and involved in tumor progression. [score:2]
The MTT assay showed that miR-452 overexpression obviously reduced MG-63 cell proliferation (Fig.   3b). [score:2]
Therefore, the potential regulatory circuitry afforded by miR-452 is enormous, and the accurate mechanisms on how miR-452 influences osteosarcoma progression need further clarification. [score:2]
The relationship between miR-452 levels and clinicopathologic parameters was analyzed by chi-square test. [score:1]
Transfection with miR-452 mimics resulted in increased miR-452 level in MG-63 cells (P < 0.001, Fig.   3a). [score:1]
miR-452 is a member of miR-224/miR-452 cluster. [score:1]
The aim of this study was to investigate the clinical significance and prognostic value of miR-452 expression in human osteosarcoma. [score:1]
After transfection with miR-452 mimics or miR-NC, the MG-63 cells were washed and resuspended in phosphate-buffered saline and then doubly stained using the Annexin V-FITC/Propidium Iodide kit (BD Biosciences, USA). [score:1]
Previous studies have reported several downstream genes of miR-452, including BMI1 [22], CDKN1B [26], IGF-1R [29], and KRAS [32]. [score:1]
In contrast to the antitumor properties mentioned above, miR-452 may act as a potential oncogene in bladder cancer and hepatocellular carcinoma [23, 25, 26]. [score:1]
The effects of miR-452 on the biological behavior of MG-63 cells. [score:1]
MG-63 cells were seeded into six-well plates and transfected with 50-nM miR-452 mimics or miR-NC using Lipofectamine 2000 (Invitrogen, USA) in accordance with the manufacturer protocol. [score:1]
a The fold change of miR-452 in osteosarcoma relative to the matched adjacent noncancerous bone tissues. [score:1]
Prognostic value of miR-452 in osteosarcoma. [score:1]
The fold change of miR-452 in osteosarcoma relative to the matched noncancerous bone tissues was determined by the 2 [−ΔΔCt] method. [score:1]
In brief, MG-63 cells were seeded in a 96-well plate, and 20 μl MTT solution (Sigma, USA) was added to the culture medium every 24 h, after transfection with miR-452 mimics or miR-NC. [score:1]
Figure  1b shows that the relative level of miR-452 in osteosarcoma specimens was significantly lower than that in corresponding noncancerous bone tissues (mean ± SD, 4.03 ± 0.96 vs. [score:1]
Then, the association of miR-452 levels with clinicopathological features and prognosis was analyzed. [score:1]
Fig. 3Effects of miR-452 on the biological behaviors of MG-63 cells. [score:1]
miR-452 mimics and negative control (miR-NC) were obtained from GenePharma (China). [score:1]
Patients with low level of miR-452 showed shorter overall survival than those with high miR-452 level. [score:1]
Then, we evaluated the prognostic significance of miR-452 expression in patients with osteosarcoma. [score:1]
[1 to 20 of 70 sentences]
3
[+] score: 84
Use of open-source software (PicTar, miRDB, and TargetScan) to predict and identify target miRNAs in this study found that the 3′UTR region of VEGF-A mRNA harbors potential binding sites for 13 candidate miRNAs, and that the greatest downregulation of miR-452 occurs after WISP-3 stimulation (Supplementary Figure 2). [score:8]
These results reveal a positive correlation between WISP-3 mRNA expression and VEGF-A (Figure 6D), while miR-452 expression was negatively correlated with WISP-3 and VEGF-A expression (Figure 6E and 6F). [score:7]
Incubation with c-Src and p38 inhibitors or siRNAs reversed WISP-3 -mediated miR-452 expression and VEGFA-3′UTR luciferase activity (Figure 4H-4K), indicating that miR-452 inhibits VEGF-A protein production through integration with the 3′UTR region of the human VEGF-A gene via the c-Src and p38 pathways. [score:7]
We also found that WISP-3 promotes the production and secretion of the angiogenic factor VEGF-A through the inhibition of miR-452 via the c-Src and p38 pathways in human chondrosarcoma cells, subsequently inducing angiogenesis in human EPCs, suggesting that WISP-3 and miR-452 may be novel molecular targets for inhibiting VEGF-A -induced angiogenesis in chondrosarcoma. [score:7]
This current study has indicated that WISP-3 markedly inhibits the expression of miR-452 in human chondrosarcoma cells in vitro and in vivo. [score:5]
Cells pretreated with pharmacologic inhibitors or pretransfected with siRNAs as indicated were then stimulated with WISP-3; miR-452 expression (n=4) (H&I) and VEGF-A promoter luciferase (n=5) (J&K) were analyzed. [score:5]
WISP-3 increases VEGF-A expression and angiogenesis by inhibiting miR-452. [score:5]
Exogenous WISP-3 inhibited miR-452 expression in a concentration -dependent manner (Figure 4A). [score:5]
In this current study, we found that WISP-3 induced VEGF-A expression and subsequently promoted angiogenesis and tumor growth in human chondrosarcoma cells via suppressing miR-452 through the c-Src and p38 signaling cascades. [score:5]
Figure 6mRNA expression of WISP-3, VEGF-A, and miR-452 in normal cartilage (n=5) and chondrosarcoma tissue (n=8) were examined by qPCR (A-C). [score:3]
Both profiles were higher in chondrosarcoma specimens than in normal cartilage (Figure 6A and 6B); lower expression of miR-452 was seen in chondrosarcoma patients (Figure 6C). [score:3]
Conversely, the miR-452 mimic also inhibited WISP-3-boosted EPC migration and tube formation (Figure 4D and 4E). [score:3]
WISP-3, VEGF-A and miR-452 expression have important clinical significance in patients with chondrosarcoma. [score:3]
mRNA expression of WISP-3, VEGF-A, and miR-452 in normal cartilage (n=5) and chondrosarcoma tissue (n=8) were examined by qPCR (A-C). [score:3]
WISP-3 promotes VEGF-A and angiogenesis via inhibition of miR-452. [score:3]
miR-452 mimic transfection diminished WISP-3-enhanced VEGF-A expression (Figures 4B and 4C). [score:3]
We also found that miR-452 directly reduced VEGF-A production via integration with the 3′UTR of the human VEGF-A gene, negatively modulating VEGF-A -induced angiogenesis. [score:2]
To investigate whether miR-452 regulated WISP-3 -induced VEGF-A expression and angiogenesis, the miR-452 mimic was used. [score:2]
Control miRNA, miR-452 mimic, MMLV RT kit, Trizol and Lipofectamine 2000 were purchased from Invitrogen (Carlsbad, CA, USA). [score:1]
Figure 4(A) Cells were incubated with WISP-3 for 24 h and the miR-452 was examined by qPCR (n=5). [score:1]
The correlations between WISP-3/VEGF-A (D), WISP-3/miR-452 (E) and VEGF-A/miR-452 (F). [score:1]
We then examined whether miR-452 controls the 3′UTR region of VEGF-A (Figure 4F). [score:1]
miR-452 mimic transfection reduced WISP-3-promoted VEGF-A production and EPC migration and tube formation. [score:1]
[1 to 20 of 23 sentences]
4
[+] score: 70
The most strongly downregulated miRNA in smokers, miR-452, had the most predicted targets with upregulated expression. [score:11]
We were particularly interested in whether the highly downregulated miRNA, miR-452, influenced the expression of MMP12, a protease relevant to smoking-related diseases that is highly upregulated in alveolar macrophages of smokers. [score:11]
Transfecting in an inhibitor of miR-452 resulted in elevated expression of MMP12 transcripts, but had no effect on another predicted target of miR-452, TM7SF4 (Figure 5). [score:7]
In experiments utilizing a miR-452 inhibitor, we show that inhibition of this miRNA in differentiated THP-1 cells resulted in elevated MMP12 transcript expression. [score:7]
In vitro experiments showed a direct link between low expression of miR-452 and increased expression of MMP12 mRNA. [score:6]
RNA was collected from PMA-differentiated THP1 cells at 24 hours post-transfection with either a control miRNA inhibitor or a miR-452 inhibitor. [score:5]
Inhibition of miRNA-452 results in increased MMP12 expression. [score:5]
Similarly, transcriptional regulation may also be important for many of the significantly repressed miRNAs in smoker alveolar macrophages because ten downregulated miRNAs were processed from four polycistronic pri-miRNAs (miR-224/miR452, miR-200a/miR-200b/miR-429, miR-449a/miR-449b/miR-449c, and let-7e/miR-99b/miR-125a). [score:5]
0044066.g005 Figure 5 RNA was collected from PMA-differentiated THP1 cells at 24 hours post-transfection with either a control miRNA inhibitor or a miR-452 inhibitor. [score:5]
Quantitative RT-PCR was used to determine the expression of putative miR-452 target. [score:5]
They were then transfected with the miR-452 or negative control mirVana miRNA Inhibitors (25 nM; ABI) using RNAiMAX (Invitrogen). [score:3]
[1 to 20 of 11 sentences]
5
[+] score: 25
While expression of some of these miRNAs seemed to be specifically dysregulated in certain tumor stages, 12 miRNAs, including 4 up-regulated (miR-200c, miR-487a, miR-491-3p and miR-452) and 8 down-regulated miRNAs (miR-125b, miR-142-3p, miR-199a-5p, miR-22, miR-299-3p, miR-29a, miR-429, and miR-532-5p), were identified to be commonly dysregulated in all ccRCC tumors at different stages (Table 1). [score:11]
Eleven commonly dysregulated miRNAs, including 3 up-regulated (miR-487a, miR-491-3p and miR-452) and 8 down-regulated (miR-125b, miR-142-3p, miR-199a-5p, miR-22, miR-299-3p, miR-29a, miR-429, and miR-532-5p), were identified in ccRCC tumor samples as compared with adjacent nontumorous samples. [score:7]
Eleven miRNAs were identified to be commonly dysregulated, including three up-regulated (miR-487a, miR-491-3p and miR-452) and eight down-regulated (miR-125b, miR-142-3p, miR-199a-5p, miR-22, miR-299-3p, miR-29a, miR-429, and miR-532-5p) in tumor tissues as compared with adjacent normal tissues. [score:7]
[1 to 20 of 3 sentences]
6
[+] score: 22
Down-regulation of miR-452 has been associated with promoting stem-like traits and tumorigenesis of gliomas and it has been suggested that it may represent a novel prognostic biomarker and therapeutic target for the disease [62]. [score:8]
In addition, 10 miRNAs; miR-720, miR-891a, miR-522, miR-518c, miR-3665, miR-3620, miR-382, miR-452, miR-122 and miR-147 were found down-regulated in the patient group, indicating tumor suppressor properties. [score:6]
Remaining in the same context, both initial and meta-analyses showed that miR-720, miR-891a, miR-3665, miR-3620, miR-382, miR-452, and miR-122 were down-regulated in the patient group and therefore indicating that they might possess tumor-suppressive activities. [score:6]
Finally, ten miRNAs were found overexpressed in the control group when compared to the patients group (relapsed or in Complete Remission (CR)); miR-720 (I), miR-891a (J), miR-522 (K), miR-518c (L), miR-3665 (M), miR-891a (N), miR-382 (O), miR-452 (P), miR-122 (Q), miR-147 (R). [score:2]
[1 to 20 of 4 sentences]
7
[+] score: 16
Among the hsa-mir-452 targets are: inhibitor of growth family member 5 (NM_032329); zinc finger and SCAN domain containing 2 (NM_ 181877) with hsa-mir-452 target sites out of Alu insertions, and Mps One Binder kinase activator-like 2A (NM_130807) with target site in an anti-sense AluYi6 insertion. [score:9]
The predicted hsa-mir-452, for which there is no information in miRNA databases, has 5 of 12 occurrences in the ‘development’ group (of them, 2 in Alu insertions), so it is very probable that its function also is related to development. [score:3]
Besides the above mentioned hsa-mir-452, the ‘cell cycle’ category contains increased number of target sites for hsa-let-7c, 7b, hsa-mir-128b, -214 and -378. [score:3]
Here we meet again hsa-mir-452. [score:1]
[1 to 20 of 4 sentences]
8
[+] score: 15
Furthermore, these 34 target-mRNAs were regulated by hsa-mir-29a, hsa-mir-29b, hsa-mir-29c, hsa-mir-452 and hsa-mir-1266, and were all related to neuronal development, neurodegenerative diseases and aging-related disorders. [score:7]
Hsa-mir-452 was reported to be over-expressed in the WNT signaling associated medulloblastomas [50]. [score:3]
The gene NAV3 was synergistically regulated by hsa-mir-29a, hsa-mir-29b, hsa-mir-29c and hsa-mir-452. [score:2]
The gene ITPKB was synergistically regulated by hsa-mir-29b and hsa-mir-452, which involved in neuronal calcium dependent signaling, a cellular process related to both AD and aging [54]. [score:2]
For example, miRNA clique 103 (Figure  7) consisted of six miRNAs: hsa-mir-29a, hsa-mir-29b, hsa-mir-1255a, hsa-mir-1266, hsa-mir-452 and hsa-mir-29c. [score:1]
[1 to 20 of 5 sentences]
9
[+] score: 11
MiR-31, miR-34b-3p, miR-205, miR-224 and miR-452 showed differential expression levels between normal, PIN and PCa matched samples (p<0.01 by Friedman test; Fig 3). [score:3]
In this analysis, reduced miRNA levels correlated with clinico-pathological progression of PCa (Table 2), and differential expression of mir-31, miR-34b-3p and miR-452 could significantly discriminate patients according to biochemical relapse (Fig 4A). [score:3]
Conversely, miR-452 and miR-224 were not differentially expressed between PCa and BPH or between PIN and BPH, respectively (Fig 4B). [score:3]
MiR-31, 34b-3p, 205, 224 and miR-452 displayed significantly altered levels between the three tissue classes (p<0.01 by Friedman test). [score:1]
B) MiR-31, 34b-3p, 205, 224 and miR-452 expression was evaluated by qPCR in unpaired pre-cancerous glands (PIN, n = 50), neoplastic prostate lesions (PCa, n = 66), or benign hyperplastic tissues (BPH, n = 10). [score:1]
[1 to 20 of 5 sentences]
10
[+] score: 11
Finally, miR-452 was upregulated in Poly (I:C) treated RAFLS. [score:4]
MiR-144*, miR-30d-3p, miR-452, miR-340, miR-202, miR-500, miR-626, miR-330-3p and miR-302c* expression was determined by RT-qPCR in RAFLS (n = 3) and SScHDF (n = 3) stimulated with Poly (I:C) (10 µg/mL) or IFN-γ (0.1 or 5 ng/mL) for 72 h. were normalized to U6snRNA and expressed as fold change compared with samples from RAFLS or SScHDF incubated with medium. [score:4]
uk/enright-srv/microcosm/htdocs/targets/v5) identified several miRNAs candidates: miR-144*, miR-452, miR-340, miR-202, miR-500, miR-626, miR-330-3p, miR-302c* and miR-30 family members (miR-30a, d and e which share the same seed sequence). [score:3]
[1 to 20 of 3 sentences]
11
[+] score: 10
For example, a mRNA of miR-452, ARMC1 is up-regulated and frequently amplified in human hepatocellular carcinoma [40]. [score:4]
miRNAs Targeted mRNAs modules miR-557ADRA1D, ACVR1C, DNAJA3, FAM120A HCV+ miR-214ASB16, GALNTL4, CBX5, BNC2, PDLIM2, RAB43, SPCS2, NKTR, ASXL1, ACLY,C6orf192, ING4, GLG1, SHOC2 HCV+ miR-34aCPLX2, FNDC5 HCV+ miR-493-3p WDR33 HCV+ miR-184EPB41L5, ALDH4A1 HCV+ miR-129 CBLB, OCRL, COMT, DENND2C HCV- miR-765ABCC5, BRD3, ANKRD12, AUTS2, PCID2, NMD3, NUP43 HCV-/+ miR-210FGD4, HDAC4, CACNA2D2, OAZ2, ADAMTS5, AK3, CDKN1B, EPM2AIP1, PPP1R12B, PRPF4B, STAM2, EZ6L, SAMD4A, PISD, KCTD9, FAM118A, CHD2, KIT, TCF4 HCV- miR-452 ARMC1, ZNF462, EFNA3, SMG5, FAM73B HCV- miR-17-3pBNC2, DICER1, GFRA1, KIAA1804, ENPP1, ZNF558, ERO1L, SNX27, ZNF718 HCV- The numbers of mRNAs in these significant modules are shown in the last column of Table 2. Figure 4 and 5 show two examples of these significant modules, and all the miRNAs in bold and the mRNAs with underline and italics can be confirmed by the literature. [score:3]
miRNAs Targeted mRNAs modules miR-557ADRA1D, ACVR1C, DNAJA3, FAM120A HCV+ miR-214ASB16, GALNTL4, CBX5, BNC2, PDLIM2, RAB43, SPCS2, NKTR, ASXL1, ACLY,C6orf192, ING4, GLG1, SHOC2 HCV+ miR-34aCPLX2, FNDC5 HCV+ miR-493-3p WDR33 HCV+ miR-184EPB41L5, ALDH4A1 HCV+ miR-129 CBLB, OCRL, COMT, DENND2C HCV- miR-765ABCC5, BRD3, ANKRD12, AUTS2, PCID2, NMD3, NUP43 HCV-/+ miR-210FGD4, HDAC4, CACNA2D2, OAZ2, ADAMTS5, AK3, CDKN1B, EPM2AIP1, PPP1R12B, PRPF4B, STAM2, EZ6L, SAMD4A, PISD, KCTD9, FAM118A, CHD2, KIT, TCF4 HCV- miR-452 ARMC1, ZNF462, EFNA3, SMG5, FAM73B HCV- miR-17-3pBNC2, DICER1, GFRA1, KIAA1804, ENPP1, ZNF558, ERO1L, SNX27, ZNF718 HCV-The numbers of mRNAs in these significant modules are shown in the last column of Table 2. Figure 4 and 5 show two examples of these significant modules, and all the miRNAs in bold and the mRNAs with underline and italics can be confirmed by the literature. [score:3]
[1 to 20 of 3 sentences]
12
[+] score: 9
Regarding the number of target mRNAs; miR-944, miR-141-3p, and miR-203a ranked top three among down-regulated miRNAs, while miR-140-3p, miR-452-5p, and miR-137 located top three of up-regulated miRNAs (Figure 1). [score:9]
[1 to 20 of 1 sentences]
13
[+] score: 9
Of the 186 miRNAs the expression of which was altered, nine were up-regulated at both time points (miR-125a-3p, miR-297c, miR-421, miR-452, miR-483, miR-574-3p, miR-574-5p, miR-669a, miR-720) and 11 were down-regulated at both time points (let-7g, miR-107, miR-10a, miR-15a, miR-15b, miR-199b*, miR-26a, miR-29c, miR-324-5p, miR-331-3p, miR-342-3p). [score:9]
[1 to 20 of 1 sentences]
14
[+] score: 9
Of these, 14 (miR-23b, miR-28, miR-98, miR-103, miR-107, miR-193a,0, miR-324-5p, miR-324-3p, miR-331, miR-374, miR-432, miR-502, and miR-660) were upregulated and 6 (miR-31, miR-451, miR-452, miR-565, miR-594 and miR-659) were downregulated. [score:7]
[27]↓quail myoblasts diff, ↓ C2C12 diff [29] ↓ C2C12 diff [28] ↓ muscle development [32]40miR-320↓(this study)↑ pMyo diff [33]  41 miR-324-3p (n)↑↑(this study)   42 miR-324-5p (n)↑(this study)   43 miR-331 (n)↑(this study)-  44miR-339↓(this study)↑ C2C12 diff [33] ↑ pMyo diff [33]  45miR-361↑(this study)↑ pMyo diff [33]  46 miR-362↑↑(this study)↑ C2C12 diff [28]  47 miR-374 (n)↑(this study)   48 miR-432 (n)↑(this study)   49 miR-451 (n)↓↓↓(this study)   50 miR-452 (n)↓↓(this study)   51 miR-500↑↑(this study)↑ C2C12 diff [28, 33] ↑ pMyo diff [33]  52 miR-501↑↑↑(this study)↑ C2C12 diff [28, 33]  53 miR-502 (n)↑↑(this study)-  54 miR-503↑(this study)↑ C2C12 diff [19, 28, 33] ↑ pMyo diff [33]  55 miR-532↑↑(this study)↑ C2C12 diff [28, 33] ↑ pMyo diff [33]  56↓↓ pMyo diff. [score:2]
[1 to 20 of 2 sentences]
15
[+] score: 8
Other miRNAs from this paper: hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-146a
Six microRNAs including miR-145, -143, -145*, -143*, -253-5p and miR-452, were up regulated after SOX2 knockdown and the rest were down regulated when SOX2 was knocked down. [score:5]
Using next generation sequencing, we identified 105 precursor microRNAs (corresponding to 95 mature miRNAs) regulated by SOX2, including down regulation of miR-143, -145, -253-5p and miR-452. [score:3]
[1 to 20 of 2 sentences]
16
[+] score: 8
This may occur through miR-452, which is highly expressed in cNC-derived mesenchyme at E10.5 in the first pharyngeal arch and regulates Fgf8 and Dlx2 expression. [score:6]
The neural crest-enriched microRNA miR-452 regulates epithelial-mesenchymal signaling in the first pharyngeal arch. [score:2]
[1 to 20 of 2 sentences]
17
[+] score: 8
Interestingly Van Schooneveld et al. [52] referred an over -expression in healthy patients compared to BC patients, and they evidenced a positive association (P < 0.05) between expression levels of miR-452 in serum of patients and the number of methylated genes in plasma. [score:4]
The experimental evidences showed a strong over -expression of miR-452 in healthy controls compared to tumour samples, and because of the evidence of the stability of this miRNA in plasma, the authors speculated a potential role as biomarker for the detection of BC in human plasma. [score:2]
The sf-hsa-miR-452 is involved in different processes as cell-cell interaction, cell growth and proliferation, inflammatory response and apoptotic processes. [score:1]
The blue rectangle evidences an inverse correlation between the mir-452 and some IDC samples. [score:1]
[1 to 20 of 4 sentences]
18
[+] score: 7
Amongst the most dysregulated miRNAs that were expressed in relatively high amounts (threshold of mean miR count > 10), miR-224-5p (-11 log [2] FC), miR-452-5p and miR-887 (both -9 log [2] FC), were significantly down-regulated, whereas the greatest relative induction was seen for miR-708-5p/3p and 3614-5p (all ~2 log [2] FC) (Fig 2C). [score:7]
[1 to 20 of 1 sentences]
19
[+] score: 7
The top 8 downregulated (hsa-miR-200c, hsa-miR-212, hsa-miR-29a, hsa-miR-532, hsa-miR-141, hsa-miR-1, hsa-miR-363, hsa-miR-187) and 8 upregulated (hsa-miR-487, hsa-miR-452, hsa-miR-1233, hsa-miR-92a, hsa-miR-106b, hsa-miR-1290, hsa-miR-320, hsa-miR-26a) miRNAs were presented in Figure 1A. [score:7]
[1 to 20 of 1 sentences]
20
[+] score: 7
Normalization of exosomal samples was conducted against an average of the expression of miR-452–5p and miR-183–5p. [score:3]
These two miRNAs were chosen as endogenous exosomal miRNAs for normalization since they were among the most frequently sequenced exosomal miRNAs in HeLa cells (> 1,000 RPM in each sample) and showed virtually no regulation in exosomes upon silencing of HPV18 E6/E7 versus control treatment based on the deep sequencing data (miR-452–5p: FC [mean] = 0.99, miR-183–5p: FC [mean] = 1.04). [score:2]
Both miRNAs were frequently sequenced (> 1,000 RPM in each sample) and showed virtually no alterations of their exosomal concentrations upon E6/E7 silencing versus control treatment (miR-452–5p: FC [mean] = 0.99, miR-183–5p: FC [mean] = 1.04). [score:1]
Therefore, two miRNAs, miR-452–5p and miR-183–5p, were chosen as stable endogenous exosomal miRNA controls based on the small RNA deep sequencing data (in analogy to refs. [score:1]
[1 to 20 of 4 sentences]
21
[+] score: 7
For example, Sun et al. found that while microRNA-223 levels were significantly enriched in HIV-1-infected CD4(+)CD8(-) PBMCs, microRNA-29a/b, microRNA-155 and microRNA-21 levels were significantly reduced [36] and Terrier et al. that four miRNAs (miR-21, miR-29a, miR-29b and miR-452) were downregulated and only one (miR-146a) upregulated in lung A549 cells upon H1N1 and H3N2 infection [35]. [score:7]
[1 to 20 of 1 sentences]
22
[+] score: 7
Especially, previous study of Puerta-Gil et al. identified miR-143, miR-222, and miR-452 as tumor stratification and noninvasive diagnostic biomarkers for BC [9]; Majid et al. [10] reported that miR-23b could function as a tumor suppressor that may confer a proliferative advantage and promote bladder cancer cell migration and invasion; Wu et al. [11] also found that miR-99a could inhibit cell proliferation, migration and invasion by targeting fibroblast growth factor receptor 3 in BC. [score:7]
[1 to 20 of 1 sentences]
23
[+] score: 6
These results indicate that miR-224 and miR-452 may be down-regulated through DNA methylation in GC cell lines as the same transcription unit. [score:4]
Figure 2a also reveals that miR-452 is clustered with miR-224. [score:1]
The DPYSL2 and KRAS mRNA levels were decreased after transfection with the miR-224 or miR-452 mimic (Figure 5B). [score:1]
[1 to 20 of 3 sentences]
24
[+] score: 5
In contrast, rCCN6 promoted angiogenesis in human chondrosarcoma cell lines SW1353 and JJ012 by induction of VEGF-A expression through inhibition of miR-452, which interacts with the 3′UTR of the human VEGF-A gene repressing its transcription [86]. [score:5]
[1 to 20 of 1 sentences]
25
[+] score: 5
Other miRNAs from this paper: hsa-mir-224, hsa-mir-141, hsa-mir-200c, hsa-mir-888, hsa-mir-877
All three microRNAs that are differentially expressed between the Xq tensor GSVD classes, and map to the same amplification, miR-888, miR-224, and miR-452, together with the gamma-aminobutyric acid (GABA) A receptor epsilon-encoding GABRE, which hosts mir-224 and mir-452 in its introns, are consistently overexpressed. [score:5]
[1 to 20 of 1 sentences]
26
[+] score: 4
Also, miR-452*, an activator in our screen, was predicted to target NFKBIE, a repressor of NF-κB signaling. [score:3]
Two of these, miR-483 and miR-452*, were hits in both screens. [score:1]
[1 to 20 of 2 sentences]
27
[+] score: 4
Other miRNAs from this paper: hsa-mir-129-1, hsa-mir-129-2, hsa-mir-423, hsa-mir-18b, hsa-mir-622
Aliquots of sera were pooled from patients with Ross scores <3, 3–5, and >5 for expression analysis of miR129-5p, miR18b, miR423-5p, miR622, and miR452. [score:3]
Following linear pre-amplification of miRNA sequences using the Applied Biosystems Preamplification system, relative expression was determined using singleplex TaqMan Assays (ABI) with primer sets for miR-129 (ABI; 000590), miR-18b (ABI; 002310), miR-423-5p (ABI; 002340), miR-622 (ABI; 001553), and miR-452 (ABI; 002330). [score:1]
[1 to 20 of 2 sentences]
28
[+] score: 3
MiRNA expression in urothelial carcinomas: important roles of miR-10a, miR-222,, miR-7 and miR-452 for tumor stage and metastasis, and frequent homozygous losses of miR-31. [score:3]
[1 to 20 of 1 sentences]
29
[+] score: 3
Differential miRNA expression levels included higher levels of MIR767, MIR135B, MIR1269, MIR182, MIR183, and MIR203 and lower levels of MIR494, MIR424, MIR381, MIR452, and MIR155 in PANC-1 cells. [score:3]
[1 to 20 of 1 sentences]
30
[+] score: 3
Other miRNAs from this paper: hsa-let-7c, hsa-let-7d, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-20a, hsa-mir-21, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-99a, hsa-mir-148a, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-181a-2, hsa-mir-181a-1, hsa-mir-125b-1, hsa-mir-143, hsa-mir-125b-2, hsa-mir-126, hsa-mir-146a, hsa-mir-155, hsa-mir-106b, hsa-mir-99b, hsa-mir-26a-2, hsa-mir-378a, hsa-mir-151a, hsa-mir-450a-1, hsa-mir-450a-2, hsa-mir-92b, hsa-mir-151b, hsa-mir-378d-2, bta-mir-26a-2, bta-let-7f-2, bta-mir-148a, bta-mir-151, bta-mir-16b, bta-mir-20a, bta-mir-21, bta-mir-26b, bta-mir-99a, bta-mir-125b-1, bta-mir-126, bta-mir-181a-2, bta-mir-92a-2, bta-let-7d, bta-mir-17, bta-mir-450a-2, bta-mir-7-3, bta-let-7f-1, bta-let-7c, bta-mir-125b-2, bta-mir-15a, bta-mir-99b, hsa-mir-450b, bta-mir-106b, bta-mir-143, bta-mir-146a, bta-mir-155, bta-mir-16a, bta-mir-26a-1, bta-mir-378-1, bta-mir-452, bta-mir-92a-1, bta-mir-92b, bta-mir-7-2, bta-mir-7-1, bta-mir-181a-1, bta-mir-2284i, bta-mir-2285a, bta-mir-2284s, bta-mir-2285d, bta-mir-2284l, bta-mir-2284j, bta-mir-2284t, bta-mir-2285b-1, bta-mir-2284d, bta-mir-2284n, bta-mir-2284g, bta-mir-2284p, bta-mir-2284u, bta-mir-2284f, bta-mir-2284a, bta-mir-2284k, bta-mir-2284c, bta-mir-2284v, bta-mir-2285c, bta-mir-2284q, bta-mir-2284m, bta-mir-2284b, bta-mir-2284r, bta-mir-2284h, bta-mir-2284o, bta-mir-2284e, bta-mir-450a-1, bta-mir-378-2, hsa-mir-378b, bta-mir-2284w, bta-mir-2284x, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, bta-mir-450b, bta-mir-2284y-1, bta-mir-2285e-1, bta-mir-2285e-2, bta-mir-2285f-1, bta-mir-2285f-2, bta-mir-2285g-1, bta-mir-2285h, bta-mir-2285i, bta-mir-2285j-1, bta-mir-2285j-2, bta-mir-2285k-1, bta-mir-2285l, hsa-mir-378j, bta-mir-2285o-1, bta-mir-2285o-2, bta-mir-2285n-1, bta-mir-2285n-2, bta-mir-2285p, bta-mir-2285m-1, bta-mir-2285m-2, bta-mir-2284y-2, bta-mir-378b, bta-mir-2285n-3, bta-mir-2285n-4, bta-mir-2284y-3, bta-mir-2285o-3, bta-mir-2285o-4, bta-mir-2285m-3, bta-mir-378c, bta-mir-2284y-4, bta-mir-2284y-5, bta-mir-2284y-6, bta-mir-2285m-4, bta-mir-2285o-5, bta-mir-2285m-5, bta-mir-2285n-5, bta-mir-2285n-6, bta-mir-2284y-7, bta-mir-2285n-7, bta-mir-2284z-1, bta-mir-2284aa-1, bta-mir-2285k-2, bta-mir-2284z-3, bta-mir-2284aa-2, bta-mir-2284aa-3, bta-mir-2285k-3, bta-mir-2285k-4, bta-mir-2284z-4, bta-mir-2285k-5, bta-mir-2284z-5, bta-mir-2284z-6, bta-mir-2284z-7, bta-mir-2284aa-4, bta-mir-2285q, bta-mir-2285r, bta-mir-2285s, bta-mir-2285t, bta-mir-2285b-2, bta-mir-2285v, bta-mir-2284z-2, bta-mir-2285g-2, bta-mir-2285g-3, bta-mir-2285af-1, bta-mir-2285af-2, bta-mir-2285y, bta-mir-2285w, bta-mir-2285x, bta-mir-2285z, bta-mir-2285u, bta-mir-2285aa, bta-mir-2285ab, bta-mir-2284ab, bta-mir-2285ac, bta-mir-2285ad, bta-mir-2284ac, bta-mir-2285ae, bta-mir-378d, bta-mir-2285ag, bta-mir-2285ah, bta-mir-2285ai, bta-mir-2285aj, bta-mir-2285ak, bta-mir-2285al, bta-mir-2285am, bta-mir-2285ar, bta-mir-2285as-1, bta-mir-2285as-2, bta-mir-2285as-3, bta-mir-2285at-1, bta-mir-2285at-2, bta-mir-2285at-3, bta-mir-2285at-4, bta-mir-2285au, bta-mir-2285av, bta-mir-2285aw, bta-mir-2285ax-1, bta-mir-2285ax-2, bta-mir-2285ax-3, bta-mir-2285ay, bta-mir-2285az, bta-mir-2285an, bta-mir-2285ao-1, bta-mir-2285ao-2, bta-mir-2285ap, bta-mir-2285ao-3, bta-mir-2285aq-1, bta-mir-2285aq-2, bta-mir-2285ba-1, bta-mir-2285ba-2, bta-mir-2285bb, bta-mir-2285bc, bta-mir-2285bd, bta-mir-2285be, bta-mir-2285bf-1, bta-mir-2285bf-2, bta-mir-2285bf-3, bta-mir-2285bg, bta-mir-2285bh, bta-mir-2285bi-1, bta-mir-2285bi-2, bta-mir-2285bj-1, bta-mir-2285bj-2, bta-mir-2285bk, bta-mir-2285bl, bta-mir-2285bm, bta-mir-2285bn, bta-mir-2285bo, bta-mir-2285bp, bta-mir-2285bq, bta-mir-2285br, bta-mir-2285bs, bta-mir-2285bt, bta-mir-2285bu-1, bta-mir-2285bu-2, bta-mir-2285bv, bta-mir-2285bw, bta-mir-2285bx, bta-mir-2285by, bta-mir-2285bz, bta-mir-2285ca, bta-mir-2285cb, bta-mir-2285cc, bta-mir-2285cd, bta-mir-2285ce, bta-mir-2285cf, bta-mir-2285cg, bta-mir-2285ch, bta-mir-2285ci, bta-mir-2285cj, bta-mir-2285ck, bta-mir-2285cl, bta-mir-2285cm, bta-mir-2285cn, bta-mir-2285co, bta-mir-2285cp, bta-mir-2285cq, bta-mir-2285cr-1, bta-mir-2285cr-2, bta-mir-2285cs, bta-mir-2285ct, bta-mir-2285cu, bta-mir-2285cv-1, bta-mir-2285cv-2, bta-mir-2285cw-1, bta-mir-2285cw-2, bta-mir-2285cx, bta-mir-2285cy, bta-mir-2285cz, bta-mir-2285da, bta-mir-2285db, bta-mir-2285dc, bta-mir-2285dd, bta-mir-2285de, bta-mir-2285df, bta-mir-2285dg, bta-mir-2285dh, bta-mir-2285di, bta-mir-2285dj, bta-mir-2285dk, bta-mir-2285dl-1, bta-mir-2285dl-2, bta-mir-2285dm
Several of the top microRNAs in RMECs, for example, miR-452 and miR-151, have not previously been reported as highly expressed in endothelial cells. [score:3]
[1 to 20 of 1 sentences]
31
[+] score: 3
In particular, Bloomston and colleagues [34], using the miRNA microarray chip OSU_CCC v. 3.0, which contains 326 human miRNA probes, identified a subgroup of six miRNAs (miR-30a-3p, miR-105, miR-127, miR-187, miR-452, and miR-518a2) that distinguish long-term survivors with node -positive disease from those succumbing within 24 months. [score:3]
[1 to 20 of 1 sentences]
32
[+] score: 3
Veerla S. Lindgren D. Kvist A. Frigyesi A. Staaf J. Persson H. Liedberg F. Chebil G. Gudjonsson S. Borg A. Mirna expression in urothelial carcinomas: Important roles of mir-10a, mir-222, mir-125b, mir-7 and mir-452 for tumor stage and metastasis, and frequent homozygous losses of mir-31 Int. [score:3]
[1 to 20 of 1 sentences]
33
[+] score: 3
A previous study from our institution had predicted eleven of these fourteen (79%) miRNAs (hsa-miR-454, has-miR-582-5p, has-miR-181d, has-miR-500, has-miR-181c, has-miR-411, has-miR-363, has-miR-381, has-miR-302c*, has-miR-652 and has-miR-452), to target CYP3A4/5/7 3’-UTR using in silico approach [29]. [score:3]
[1 to 20 of 1 sentences]
34
[+] score: 3
MiRNA expression in urothelial carcinomas: important roles of miR-10a, miR-222, miR-125b, miR-7 and miR-452 for tumor stage and metastasis, and frequent homozygous losses of miR-31. [score:3]
[1 to 20 of 1 sentences]
35
[+] score: 3
Ten miRNAs (let-7e, miR-128, miR-323-3p, miR-133b, miR-18b, miR-144, miR-451, miR-150, miR-486-3p, and miR-196b-5p) reflected a fourfold differential expression, and three miRNAs (miR-130b-5p, miR-452, and miR-579) were only identified in plasma from RA patients. [score:3]
[1 to 20 of 1 sentences]
36
[+] score: 3
Circular RNAs Target microRNAs Name Gene Name Number of seed matches Refs in gastric cancer hsa_circ_0001340 TMCC1 hsa-miR-452–5p 1 [30,31] hsa_circ_0000419 RAB3IP hsa-miR-145–5p 1 [32–34] hsa_circ_0001112 DGKD hsa-miR-375 3 [35–37] hsa_circ_0000284 HIPK3 hsa-miR-224–5p 1 [31,38] hsa_circ_0000437 CORO1C hsa-miR-1 1 [39] Figure 3Simulation of the relation between CORO1C, hsa_circ_0000437 and hsa-miR-1. Pol II: RNA polymerase II. [score:3]
[1 to 20 of 1 sentences]
37
[+] score: 3
Other miRNAs from this paper: hsa-mir-21, hsa-mir-221, hsa-mir-125b-1, hsa-mir-125b-2, hsa-mir-424
Several dysregulated miRNAs, including miR-221, miR-21, miR-452, miR-424 and miR-125b, have been demonstrated to regulate HCC cell growth, apoptosis, migration and/or invasion (9– 13). [score:3]
[1 to 20 of 1 sentences]
38
[+] score: 3
MiRNA expression in urothelial carcinomas: important roles of miR-10a, miR-222, miR-125b, miR-7 and miR-452 for tumor stage and metastasis, and frequent homozygous losses of miR-31. [score:3]
[1 to 20 of 1 sentences]
39
[+] score: 2
Three miRNAs (miR-31, miR-4506, miR-452*) were differentially expressed in adenoma compared to normal both in tissue and plasma samples. [score:2]
[1 to 20 of 1 sentences]
40
[+] score: 2
MicroRNA-452 promotes stem-like cells of hepatocellular carcinoma by inhibiting Sox7 involving Wnt/-catenin signaling pathway. [score:2]
[1 to 20 of 1 sentences]
41
[+] 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-17, hsa-mir-18a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-21, hsa-mir-23a, hsa-mir-31, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-96, hsa-mir-98, hsa-mir-99a, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-99a, mmu-mir-127, mmu-mir-128-1, mmu-mir-136, mmu-mir-142a, mmu-mir-145a, mmu-mir-10b, mmu-mir-182, mmu-mir-183, mmu-mir-187, mmu-mir-193a, mmu-mir-195a, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-139, hsa-mir-10b, hsa-mir-182, hsa-mir-183, hsa-mir-187, hsa-mir-210, hsa-mir-216a, hsa-mir-217, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-224, hsa-mir-200b, mmu-mir-302a, mmu-let-7d, mmu-mir-106a, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-128-1, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-127, hsa-mir-136, hsa-mir-193a, hsa-mir-195, hsa-mir-206, mmu-mir-19b-2, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-96, mmu-mir-98, hsa-mir-200c, mmu-mir-17, mmu-mir-139, mmu-mir-200c, mmu-mir-210, mmu-mir-216a, mmu-mir-219a-1, mmu-mir-221, mmu-mir-222, mmu-mir-224, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-217, hsa-mir-200a, hsa-mir-302a, hsa-mir-219a-2, mmu-mir-219a-2, hsa-mir-363, mmu-mir-363, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-371a, hsa-mir-18b, hsa-mir-20b, mmu-mir-452, ssc-mir-106a, ssc-mir-145, ssc-mir-216-1, ssc-mir-217-1, ssc-mir-224, ssc-mir-23a, ssc-mir-183, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-128-1, ssc-mir-136, ssc-mir-139, ssc-mir-18a, ssc-mir-21, hsa-mir-146b, hsa-mir-493, hsa-mir-495, hsa-mir-497, hsa-mir-505, mmu-mir-20b, hsa-mir-92b, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, hsa-mir-671, mmu-mir-216b, mmu-mir-671, mmu-mir-497a, mmu-mir-495, mmu-mir-146b, mmu-mir-708, mmu-mir-505, mmu-mir-18b, mmu-mir-493, mmu-mir-92b, hsa-mir-708, hsa-mir-216b, hsa-mir-935, hsa-mir-302e, hsa-mir-302f, ssc-mir-17, ssc-mir-210, ssc-mir-221, mmu-mir-1839, ssc-mir-146b, ssc-mir-206, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-128-2, ssc-mir-143, ssc-mir-10b, ssc-mir-23b, ssc-mir-193a, ssc-mir-99a, ssc-mir-98, ssc-mir-92a-2, ssc-mir-92a-1, ssc-mir-92b, ssc-mir-142, ssc-mir-497, ssc-mir-195, ssc-mir-127, ssc-mir-222, ssc-mir-708, ssc-mir-935, ssc-mir-19b-2, ssc-mir-19b-1, ssc-mir-1839, ssc-mir-505, ssc-mir-363-1, hsa-mir-219b, hsa-mir-371b, ssc-let-7a-2, ssc-mir-18b, ssc-mir-187, ssc-mir-218b, ssc-mir-219a, mmu-mir-195b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-31, ssc-mir-182, ssc-mir-216-2, ssc-mir-217-2, ssc-mir-363-2, ssc-mir-452, ssc-mir-493, ssc-mir-671, mmu-let-7k, ssc-mir-7138, mmu-mir-219b, mmu-mir-216c, mmu-mir-142b, mmu-mir-497b, mmu-mir-935, ssc-mir-9843, ssc-mir-371, ssc-mir-219b, ssc-mir-96, ssc-mir-200b
adj ssc-miR-21 -1.1788 1.45E-02 1.68E-02 -2.4642 2.07E-04 3.85E-04 ssc-miR-143-3p -1.1940 1.40E-02 1.67E-02 -2.7004 2.27E-05 5.34E-05 ssc-miR-145-3p -1.2289 2.47E-02 2.68E-02 -2.6837 6.34E-04 1.10E-03 ssc-miR-505 -1.3657 2.68E-02 2.82E-02 -2.1577 4.16E-02 4.16E-02 ssc-miR-98 -1.5185 3.46E-03 5.15E-03 -2.8061 7.55E-05 1.55E-04 ssc-miR-139-3p -1.6685 2. 54E-02 2.71E-02 -2.5158 1.69E-02 1.93E-02 ssc-miR-23b -1.7157 3.70E-03 5.42E-03 -2.3687 8.39E-03 1.10E-02 ssc-miR-224 -1.8515 1.41E-02 1.67E-02 -2.5778 1.95E-02 2.19E-02 ssc-miR-23a -1.8753 3.40E-03 5.15E-03 -2.4676 1.00E-02 1.24E-02 ssc-miR-143-5p -1.9243 1.15E-04 2.60E-04 -3.9943 1.25E-09 5.88E-09 ssc-miR-139-5p -2.1198 2.01E-02 2.24E-02 -3. 2644 1.01E-02 1.24E-02 ssc-miR-222 -2.2666 2.58E-07 1.02E-06 -2.6019 2.34E-05 5.35E-05 ssc-miR-671-5p -2.3068 1.15E-02 1.47E-02 -2.7986 3.86E-02 3.92E-02 ssc-miR-9843-3p -2.3507 9.68E-04 1.87E-03 -4.7281 5.90E-05 1.31E-04 ssc-miR-145-5p -2.7059 2.08E-03 3.50E-03 -4.3459 7.18E-05 1.51E-04 ssc-miR-221-5p -2.7136 3.21E-07 1.21E-06 -1.9513 3.02E-02 3. 22E-02 ssc-miR-221-3p -2.9643 8.31E-11 5.47E-10 -2.1967 1.74E-03 2.90E-03 ssc-miR-708-5p -4.0615 2.31E-06 7.60E-06 -2.8238 6.43E-03 8.72E-03 ssc-miR-193a-3p -4.1933 2.39E-07 1.02E-06 -4.3848 2.87E-07 9.18E-07 ssc-miR-193a-5p -4.1933 2.39E-07 1.02E-06 -7.1423 2.32E-12 1.33E-11 ssc-miR-452 -4.3025 5.55E-11 3.99E-10 -2.2057 1.53E-02 1.77E-02 ssc-miR-206 -5.3001 6. 39E-09 3.37E-08 -6.2200 3.10E-09 1.38E-08 10.1371/journal. [score:1]
adj ssc-miR-21 -1.1788 1.45E-02 1.68E-02 -2.4642 2.07E-04 3.85E-04 ssc-miR-143-3p -1.1940 1.40E-02 1.67E-02 -2.7004 2.27E-05 5.34E-05 ssc-miR-145-3p -1.2289 2.47E-02 2.68E-02 -2.6837 6.34E-04 1.10E-03 ssc-miR-505 -1.3657 2.68E-02 2.82E-02 -2.1577 4.16E-02 4.16E-02 ssc-miR-98 -1.5185 3.46E-03 5.15E-03 -2.8061 7.55E-05 1.55E-04 ssc-miR-139-3p -1.6685 2. 54E-02 2.71E-02 -2.5158 1.69E-02 1.93E-02 ssc-miR-23b -1.7157 3.70E-03 5.42E-03 -2.3687 8.39E-03 1.10E-02 ssc-miR-224 -1.8515 1.41E-02 1.67E-02 -2.5778 1.95E-02 2.19E-02 ssc-miR-23a -1.8753 3.40E-03 5.15E-03 -2.4676 1.00E-02 1.24E-02 ssc-miR-143-5p -1.9243 1.15E-04 2.60E-04 -3.9943 1.25E-09 5.88E-09 ssc-miR-139-5p -2.1198 2.01E-02 2.24E-02 -3. 2644 1.01E-02 1.24E-02 ssc-miR-222 -2.2666 2.58E-07 1.02E-06 -2.6019 2.34E-05 5.35E-05 ssc-miR-671-5p -2.3068 1.15E-02 1.47E-02 -2.7986 3.86E-02 3.92E-02 ssc-miR-9843-3p -2.3507 9.68E-04 1.87E-03 -4.7281 5.90E-05 1.31E-04 ssc-miR-145-5p -2.7059 2.08E-03 3.50E-03 -4.3459 7.18E-05 1.51E-04 ssc-miR-221-5p -2.7136 3.21E-07 1.21E-06 -1.9513 3.02E-02 3. 22E-02 ssc-miR-221-3p -2.9643 8.31E-11 5.47E-10 -2.1967 1.74E-03 2.90E-03 ssc-miR-708-5p -4.0615 2.31E-06 7.60E-06 -2.8238 6.43E-03 8.72E-03 ssc-miR-193a-3p -4.1933 2.39E-07 1.02E-06 -4.3848 2.87E-07 9.18E-07 ssc-miR-193a-5p -4.1933 2.39E-07 1.02E-06 -7.1423 2.32E-12 1.33E-11 ssc-miR-452 -4.3025 5.55E-11 3.99E-10 -2.2057 1.53E-02 1.77E-02 ssc-miR-206 -5.3001 6. 39E-09 3.37E-08 -6.2200 3.10E-09 1.38E-08 10.1371/journal. [score:1]
[1 to 20 of 2 sentences]
42
[+] score: 1
Among the decreased miRNAs (Table 3), miR-451 (Rank 1), miR-144 (Rank 2), and miR-144* (Rank 15) were clustered; and miR-452 (Rank 3) and miR-224 (Rank 5) were also clustered. [score:1]
[1 to 20 of 1 sentences]
43
[+] score: 1
The opposite example is the pair hsa-miR-892c-3p and hsa-miR-452-5p. [score:1]
[1 to 20 of 1 sentences]
44
[+] score: 1
Individual miRNA assays were performed on total RNA from the initial tumor samples to determine the expression levels of miR-135b, miR-150, miR-452-5p and miR-652 when compared to normal human osteoblasts. [score:1]
[1 to 20 of 1 sentences]
45
[+] score: 1
Notably, the normal MMI-network (1738 nodes and 32375 edges) is marked by a clear segregation into two internally well connected components: a larger one (1354 nodes and 31417 edges) mainly dominated by the mir-200 family and a smaller one (378 nodes and 954 edges) mainly controlled by mir-452. [score:1]
[1 to 20 of 1 sentences]
46
[+] score: 1
Regarding miRNA-451 and miRNA-452 no differences were found. [score:1]
[1 to 20 of 1 sentences]
47
[+] score: 1
For instance, miR-143, miR-222, and miR-452 detected in urinary specimens were clinically useful for noninvasive bladder cancer diagnostics [10], and miR-9, miR-182, and miR-200b was found to be related to bladder tumor aggressiveness and survival [11]. [score:1]
[1 to 20 of 1 sentences]
48
[+] score: 1
Similarly let-7i, hsa-miR-181b, hsa-miR-21, hsa-miR-23a, hsa-miR-29a, hsa-miR-30a, hsa-miR-31 and hsa-miR-452 associated significantly with mitochondria of HeLa. [score:1]
[1 to 20 of 1 sentences]