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48 publications mentioning hsa-mir-330

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-330. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 263
Other miRNAs from this paper: mmu-mir-330
Our results showed that the SH3GL2 (−) & pre-miR-330 group showed a decreased expression of apoptotic protein Caspase-3 and TRAIL, and an increased expression of anti-apoptotic protein XIAP and Bcl-2. On the contrary, SH3GL2 (+) & anti-miR-330 group showed an increased expression of apoptotic protein Caspase-3 and TRAIL, and a decreased expression of anti-apoptotic protein XIAP and Bcl-2. This indicated that miR-330 could promote the malignant behavior of GSCs and regulate the expression of apoptotic protein through down -regulating the expression of SH3GL2 and activating ERK and PI3K/AKT signaling pathways. [score:15]
All the results indicated that the expression of miR-330 could inhibit SH3GL2 expression at protein level. [score:7]
Expression of SH3GL2 in GSCs and non-GSCs, and SH3GL2 expression with expression of miR-330 changed. [score:7]
Those stable transfected cells co -transfected with miR-330 mimics (or miR-330 inhibitors) were divided into 5 groups: control group, SH3GL2 (−) & pre-miR-330 group (SH3GL2 (−) stable cells co -transfected with miR-330 mimics), SH3GL2 (−) & anti-miR-330 group (SH3GL2 (−) stable cells co -transfected with miR-330 inhibitors), SH3GL2 (+) & pre-miR-330 group (SH3GL2 (+) stable cells co -transfected with miR-330 mimics), SH3GL2 (+) & anti-miR-330 group (SH3GL2 (+) stable cells co -transfected with miR-330 inhibitors). [score:7]
MiR-330 Inhibited the GSCs Apoptosis by Regulating the Expression of Apoptotic Proteins through Down -regulating SH3GL2. [score:6]
The Over-expressed MiR-330 Inhibited the Expression of SH3GL2 in GSCs. [score:6]
Over-expressed miR-330 could promote cell proliferation, anti-apoptosis, migration and invasion of GSCs through down -regulating SH3GL2 expression. [score:6]
To elucidate the regulation of miR-330 on SH3GL2 expression, GSCs were transfected with miR-330 mimics or miR-330 inhibitors. [score:6]
GSCs transfected with miRNAs were divided into 5 groups: control group given no miRNAs, mock 1 group transfected with miR-330 mimics negative control molecules, pre-miR-330 group transfected with miR-330 mimics, mock 2 group transfected with miR-330 inhibitors negative control molecules, anti-miR-330 group transfected with miR-330 inhibitors. [score:5]
0095060.g007 Figure 7(A) The expression levels of caspase-3 and TRAIL in GSCs with the expression of miR-330 and SH3GL2 changed. [score:5]
Expression of p-ERK/ERK and PI3K/AKT in GSCs with the expression of miR-330 and SH3GL2 changed. [score:5]
The results indicated that miR-330 could inhibit SH3GL2 expression at protein level. [score:5]
Knockdown MiR-330 and Over-expressed SH3GL2 Suppressed Tumor Growth and Prolonged Survival in vivo. [score:5]
Expression levels of apoptotic proteins in GSCs with the expression of miR-330 and SH3GL2 changed. [score:5]
However, the expression of SH3GL2 was lower in GSCs, and could be inhibited by miR-330. [score:5]
0095060.g006 Figure 6(A) The expression levels of p-ERK/ERK with the expression of miR-330 and SH3GL2 changed. [score:5]
As shown in Figure 7A, the results demonstrated that the protein expression levels of Caspase-3 and TRAIL were inhibited in SH3GL2 (−) & pre-miR-330 group compared with the control group (P<0.05). [score:4]
These results demonstrated that miR-330 inhibited apoptosis of GSCs by down -regulating SH3GL2. [score:4]
This result strongly indicated that over -expression of miR-330 could increase the malignant behavior of GSCs via the down -regulating SH3GL2. [score:4]
Meanwhile, Bcl-2 and XIAP expression was inhibited in SH3GL2 (+) & anti-miR-330 group compared with SH3GL2 (−) & pre-miR-330 group (P<0.05). [score:4]
To further clarify the potential mechanisms in the SH3GL2 -dependent regulation of malignant behavior of GSCs, the detection of ERK and PI3K/AKT activity was carried out by Western blot after the expression of miR-330 and SH3GL2 were changed. [score:4]
By contrast, the anti-miR-330 group displayed the opposite effect on SH3GL2 expression to pre-miR-330 group: the expression level of SH3GL2 was increased compared with that of the mock 2 group (P<0.05). [score:4]
To analyze miR-330 expression levels among different groups, the real-time PCR assay was used to quantify the miRNAs expression levels. [score:4]
The results proved that ERK and PI3K/AKT signaling pathways were involved in the oncogenic progression of GSCs since miR-330 negatively regulated the expression of SH3GL2. [score:4]
The in vivo studies also showed that mice carrying knockdown miR-330 and over-expressed SH3GL2 tumors produced significantly smallest tumors and had a highest survival. [score:4]
These phenomena indicated that JNK and WNT signaling pathway might be also involved in oncogenic progression of GSCs since miR-330 negatively regulated the expression of SH3GL2. [score:4]
The miR-330 knockdown plasmid, pEGFP-miR-330 -inhibitor sponge (GenePharma, Shanghai, China), was transfected using Lipofectamine LTX and Plus Reagents and selected by the culture medium containing 10 µg/ml blasticidin (Life Technologies Corporation, Carlsbad, CA, USA) to generate miR-330 (−) stable transfected cell lines. [score:4]
To determine whether apoptotic proteins were involved in the GSCs apoptosis induced by miR-330 via the down-regulation of SH3GL2, the protein expression levels of apoptotic proteins were measured by Western blot where GAPDH was used as an internal loading control. [score:4]
The in vivo studies also confirmed that mice carrying knockdown miR-330 and over-expressed SH3GL2 tumors produced significantly smallest tumors and had a highest survival. [score:4]
These results strongly suggested that miR-330 was an oncogenic factor that was involved in the migration and invasion of GSCs via down -regulating SH3GL2 expression. [score:4]
This study proved for the first time that the tumor suppressor SH3GL2 is negatively regulated by miR-330 in GSCs. [score:4]
Relative expression levels of miR-330 in GSCs and non-GSCs. [score:3]
of real-time PCR analysis showed that the miR-330 expression level was significantly higher in GSCs than non-GSCs (Figure 2). [score:3]
Results of real-time PCR analysis showed that the miR-330 expression level was significantly higher in GSCs than non-GSCs (Figure 2). [score:3]
In this study, we mainly aimed to investigate the role of miR-330 in biological significance of GSCs and thereby to determine whether the ERK and PI3K/AKT pathways will be involved in miR-330 -dependent regulation of malignant behavior of GSCs via down -regulating SH3GL2 expression. [score:3]
The expression of miR-330 in non-GSCs accounted for 45.26% of that in GSCs. [score:3]
0095060.g002 Figure 2Relative expression levels of miR-330 in GSCs and non-GSCs. [score:3]
0095060.g005 Figure 5(A) The ability proliferation in GSCs with the expression of miR-330 and SH3GL2 changed. [score:3]
The Expression of miR-330 was Increased in GSCs. [score:3]
The miRNA-330 mimics, miRNA-330 inhibitors and their negative control molecules were synthesized (Life Technologies Corporation, MD, USA). [score:3]
To generate SH3GL2 (+) & miR-330 (−) stable transfected cell lines, pEGFP-miR-330 -inhibitor sponge plasmids was transfected in SH3GL2 (+) stable transfected cells and selected by the culture medium containing 10 µg/ml blasticidin. [score:3]
Further, we investigated whether the changed expression levels of miR-330 and SH3GL2 might affect the expression of apoptotic proteins in GSCs. [score:3]
Proliferation, apoptosis, migration and invasion of GSCs with the expression of miR-330 and SH3GL2 changed. [score:3]
Expression of miR-330 in GSCs and non-GSCs. [score:3]
Proliferation, apoptosis, migration and invasion of GSCs transfected with miR-330 mimics (or miR-330 inhibitors). [score:3]
The protein expression levels of SH3GL2 in pre-miR-330 group were decreased while that it in anti-miR-330 group were increased. [score:3]
In the present study, we have found that miR-330 had a higher expression level in GSCs, which indicated that it played an oncogenic role in the GSCs. [score:3]
However, the function and molecular mechanisms of miR-330 in the regulation of GSCs malignant behavior have still remained completely unknown. [score:2]
As shown in Figure 4B, the protein expression levels of SH3GL2 were decreased in the pre-miR-330 group compared with the mock 1 group (P<0.05). [score:2]
These results demonstrated that miR-330 promoted GSCs proliferation by down -regulating SH3GL2. [score:2]
These data confirmed that miR-330 played an anti-apoptotic role in GSCs by down -regulating SH3GL2. [score:2]
The expression of p-ERK/ERK was decreased in SH3GL2 (+) & anti-miR-330 group compared with SH3GL2 (−) & pre-miR-330 group (P<0.05) (Figure 6A). [score:2]
MiR-330 was first discovered by Weber [11] and was reported to act as a tumor-suppressor in prostate and lung primary tumors [12], [13], [14]. [score:2]
Published article from our lab has shown that miR-330 could directly bind to the 3′-UTR of SH3GL2 [29]. [score:2]
The results showed that there was an increase of p-ERK/ERK expression in SH3GL2 (−) & pre-miR-330 group compared with the control group, and a decrease in SH3GL2 (+) & anti-miR-330 group. [score:2]
As shown in Figure 7B, the analysis of anti-apoptotic protein showed that the protein expression levels of XIAP and Bcl-2 were promoted in SH3GL2 (−) & pre-miR-330 group compared with the control group (P<0.05). [score:2]
These results demonstrated that the mechanism of miR-330 induced malignant behavior of GSCs was associated with the activation of ERK and PI3K/AKT pathways via down -regulating SH3GL2. [score:2]
The protein expression levels of Caspase-3 and TRAIL in SH3GL2 (+) & anti-miR-330 group were significantly promoted compared with SH3GL2 (−) & pre-miR-330 group (P<0.05). [score:2]
However, the expression of them in SH3GL2 (+) & anti-miR-330 group showed an increase compared with the control group (P<0.05). [score:2]
Data demonstrated that SH3GL2 was negatively regulated by miR-330 in GSCs, which promoted the malignant behavior of GSCs. [score:2]
However, the expression of them in SH3GL2 (+) & anti-miR-330 group showed a decrease compared with the control group (P<0.05). [score:2]
In this study, we proved that the expression level of miR-330 was increased in GSCs compared with non-GSCs. [score:2]
In order to investigate whether SH3GL2 was involved in the miR-330 -induced regulation of the malignant behavior of GSCs, the expression level of miR-330 and SH3GL2 were altered. [score:2]
0095060.g003 Figure 3(A) CCK8 assay showed that the ability of GSCs proliferation with the expression of miR-330 changed. [score:2]
SH3GL2 (−) & pre-miR-330 group. [score:1]
Result showed that GSCs treated with SH3GL2 (+) & anti-miR-330 showed lower abilities of proliferation, anti-apoptosis, migration and invasion than GSCs treated with SH3GL2 (−) & pre-miR-330. [score:1]
The expression levels of miR-330 were normalized with the reference U6, and fold changes were calculated by relative quantification (2 [−ΔΔCt]) method. [score:1]
Besides, miR-330 could promote the ability of proliferation, anti-apoptosis, migration and invasion in GSCs. [score:1]
On the contrary, the lowest activity of ERK and PI3K/AKT appeared in SH3GL2 (+) & anti-miR-330 group. [score:1]
MiR-330 Induced the Activation of ERK and PI3K/AKT Pathways by Down -regulating SH3GL2. [score:1]
Conversely, GSCs treated with SH3GL2 (−) & pre-miR-330 had higher abilities of these. [score:1]
These results clearly revealed that miR-330 could enhance FBS -induced migration and invasion of GSCs. [score:1]
The mice were randomly divided into four groups: control group given only GSC cells, SH3GL2 (+) group given the SH3GL2 (+) stable transfected cells, miR-330 (−) group given the miR-330(−) stable transfected cells, SH3GL2 (+) & miR-330 (−) group given the SH3GL2 (+) & miR-330 (−) stable transfected cell lines. [score:1]
by Down -regulating SH3GL2As shown in Figure 5A, the cellular viability of the SH3GL2 (−) & pre-miR-330 group was increased whereas that of SH3GL2 (+) & anti-miR-330 group was decreased compared with the control group. [score:1]
The results showed that GSCs treated with pre-miR-330 promoted the abilities of proliferation, anti-apoptosis, migration and invasion. [score:1]
Furthermore, the cellular viability was obviously lower in SH3GL2 (+) & anti-miR-330 group than SH3GL2 (−) & pre-miR-330 group (P<0.05). [score:1]
There was no significant difference between the SH3GL2 (+) group and the miR-330 (−) group. [score:1]
The smallest tumor sizes were observed in SH3GL2 (+) & miR-330 (−) group (P<0.05). [score:1]
MiR-330 Promoted Proliferation, Anti-apoptosis, Migration and Invasion of GSCs by Down -regulating SH3GL2. [score:1]
showed that the highest activity of ERK and PI3K/AKT appeared in SH3GL2 (−) & pre-miR-330 group. [score:1]
The apoptosis rates in mock 2 and anti-miR-330 groups were 11.2±1.58% and 17.2±2.04% respectively. [score:1]
miR-330 (−) group. [score:1]
To determine whether miR-330 was associated with GSCs apoptosis, quantization of apoptosis was assessed using flow cytometry. [score:1]
As shown in Figure 3B, the apoptosis rates in mock 1 and pre-miR-330 groups were 10.3±1.32% and 5.2±0.97% respectively. [score:1]
Conversely, the GSCs treated with anti-miR-330 had lower abilities of malignant behavior mentioned above. [score:1]
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2
[+] score: 202
The common targets of miR-330 predicted by computer-aided algorithms were obtained from multiple target prediction programs: Targetscan and Miranda (http://www. [score:7]
All of these results indicate that miR-330 post-transcriptionally inhibits SH3GL2 expression and miR-330 is negatively correlated with SH3GL2 protein expression in glioblastoma cells. [score:7]
The recent prediction of miR-330 targeting SH3GL2 3′-UTR has led our further study on the mechanism of downregulation of SH3GL2 gene in glioblastoma. [score:6]
Hodzic reported that miR-330 post-transcriptionally regulated the expression of deoxycytidine kinase by targeting its 3′-UTR and decreased its sensitivity to gemcitabine in cancer cells [36]. [score:6]
As shown in Figure 1, the expression levels of miR-330 normalized to U6 were significantly up-regulated in five glioblastoma tissues and three glioblastoma cells when compared to the three normal brain tissues. [score:5]
Previous studies show that miR-330 was able to acts as tumor suppressor and induced apoptosis of prostate cancer cells through E2F1 -mediated suppression of Akt phosphorylation [11]. [score:5]
We also showed that overexpression of miR-330 played an oncogenic role by inhibiting SH3GL2 and affected cell proliferation, migration, invasion and activation of cell cycle in U87 and U251 cells. [score:5]
The expression level of SH3GL2 and β-actin in U87 and U251 cells transfected with exogenous miR-330 or its inhibitor were analyzed by Western blot 48 h after transfection. [score:5]
0046010.g003 Figure 3 (A) Overexpression of miR-330 or transfection of exogenous miR-330 inhibitor did not change the SH3GL2 mRNA level detected by RT-PCR. [score:5]
Overexpression of miR-330 decreased luciferase activity of this reporter to about 60% of the control level (Figure 2C), suggesting that miR-330 inhibits the 3′-UTR function of SH3GL2. [score:5]
This result indicates that miR-330 is up-regulated in glioblastoma. [score:4]
Here, for the first time, we uncovered a comprehensive analysis of the regulation of miR-330 and SH3GL2 expression in glioblastoma. [score:4]
In line with the previous studies, these results indicated that miR-330 functioned as an oncogenic miRNA by negatively regulating the candidate tumor suppressor gene SH3GL2 in human glioblastoma cells. [score:4]
To further confirm the biological behavior change of glioblastoma cells through miR-330′s regulation of SH3GL2, we also transfected the siRNA targeting on SH3GL2 and got similar results as miR-330. [score:4]
In conclusion, this is the first study to show that the tumor suppressor gene SH3GL2 is negatively regulated by miR-330 at the posttranscriptional level. [score:4]
MiR-330 Post-transcriptionally Inhibited SH3GL2 Expression. [score:4]
To analyze miR-330 expression levels, the stem-loop RT-PCR assay was used to quantify the miRNAs expression levels. [score:4]
These results indicate that SH3GL2 is a direct target of miR-330 with the specific binding site at the seed sequence. [score:4]
Though, by targeting different gene and maybe through different pathways, miR-330 seems to exert the same effect in this report and our study to some extent. [score:3]
MiR-330 is a potential novel oncogenic miRNA in glioblastoma and provides a new therapeutic target of human glioblastoma. [score:3]
Meanwhile, we revealed that overexpression of miR-330 could increase the viability of glioblastoma cells. [score:3]
0046010.g001 Figure 1 Relative miR-330 expression levels were analyzed by qRT-PCR in normal brain tissues, glioblastoma tissues and established glioblastoma cell lines. [score:3]
By transfection of exogenous miR-330, we detected a reduction of SH3GL2 protein expression in two glioblastoma cells. [score:3]
Those transfected with miRNA precursors were divided into 5 groups: mock group with no miRNA precursor but PBS, pre-miR-con group with pre-miR negative control precursor, pre-miR-330 group with miR-330 precursor, anti-miR-con with anti-miR negative control precursor and anti-miR-330 group with miR-330 inhibitor precursor. [score:3]
To test whether miR-330 specifically inhibited SH3GL2 by its potential binding site of seed sequence, the mutated reporter at miR-330 binding site was constructed (Figure 2B). [score:3]
We found that there was a binding site of miR-330 in the 3′-UTR of SH3GL2, suggesting SH3GL2 as a potential target of miR-330. [score:3]
The effect of miR-330 expression on cell apoptosis was assessed by Annexin V-FITC/PI staining. [score:3]
When cell lines were transfected with exogenous miR-330 and its inhibitors, the level of SH3GL2 protein was detected by western blotting. [score:3]
Relative miR-330 expression levels were analyzed by qRT-PCR in normal brain tissues, glioblastoma tissues and established glioblastoma cell lines. [score:3]
To confirm that the overexpression of miR-330 was associated with apoptosis, we examined the apoptosis of the cells by flow cytometry 72 h after transfection. [score:3]
The expression levels of miR-330 were normalized with reference to expression levels of U6, and fold changes were calculated by relative quantification (2 [−ΔΔCt]). [score:3]
As shown in Figure 3, miR-330 induced a significant decrease of SH3GL2 protein expression without influence on mRNA level. [score:3]
These data suggest that overexpression of miR-330 cause acceleration of cell cycle through influencing SH3GL2 gene. [score:3]
A recent study showed that miR-330 induced apoptosis in prostate cancer cells through E2F1 -mediated suppression of Akt phosphorylation [11]. [score:3]
MiR-330 regulated SH3GL2 expression at the post-transcriptional level. [score:3]
The relationship between miR-330 level and SH3GL2 expression was analyzed in U87 and U251 cells. [score:3]
Forced expression of miR-330 did not affect the mutant SH3GL2 reporter activities (Figure 2D). [score:3]
MiR-330 Directly Targeted the 3′-UTR of SH3GL2. [score:3]
The expression levels of miR-330 were analyzed using RT-PCR and quantitative real-time PCR. [score:3]
What’s more, the anti-miR-330 played the opposite effect of pre-miR-330 with an increasing level of SH3GL2 protein expression versus either pre-miR-330 or anti-miR-con group (P<0.05). [score:3]
Glioblastoma cells transfected with anti-miR-330 showed higher expression of SH3GL2 protein level. [score:3]
MiR-330 Expression was Increased in Glioblastoma. [score:2]
MiR-330 Inhibited the Apoptosis of Glioblastoma. [score:2]
We observed that miR-330 overexpression enhanced FBS -induced migration ability of glioblastoma cells compared with pre-miR-con group (P<0.05) (Figures 5A and 5C). [score:2]
MiR-330 was overexpressed in human glioblastoma tissues and cells. [score:2]
Subsequently, luciferase reporter assay confirmed the prediction of miR-330′s targeting on the 3′-UTR of SH3GL2 gene. [score:2]
MiR-330 inhibited apoptosis of U87 and U251 cells. [score:2]
We found that miR-330 could influence the proliferation, migration, invasion, cell cycle and apoptosis of human glioblastoma by regulating SH3GL2 gene. [score:2]
To examine whether overexpression of miR-330 affected the migration and invasion capacity of glioblastoma cells, transwell assays were introduced. [score:2]
Our study showed that exogenous overexpression of miR-330 caused some opposite biological behavior changes in glioblastoma cells compared with those in prostate cancer cells. [score:2]
These data confirm that miR-330 plays an antiapoptotic role in glioblastoma cells by regulating SH3GL2 gene. [score:2]
These results above strongly suggest that miR-330 is an important factor involved in the migration and invasion of glioblastoma cells by regulating SH3GL2 gene. [score:2]
Cell cycle distribution of U87 and U251 cells transfected with pre-miR-con and pre-miR-330. [score:1]
We also found that miR-330 obviously increased migration and invasion of glioblastoma cells. [score:1]
However, the function and molecular mechanism of miR-330 in determining the malignant phenotype of human glioblastoma are less elusive. [score:1]
Besides, miR-330 could also influence the cell cycle and act as an antiapoptotic factor in both cell lines. [score:1]
After cultured overnight, cells were co -transfected with the wild-type or mutated SH3GL2 3′-UTR reporter plasmid, and transfected with pre-miR-330 or pre-miR-con precursors. [score:1]
These results demonstrate that miR-330 can promote cellular proliferation in glioblastoma cells in an SH3GL2 -dependent way. [score:1]
What’ more, we found the opposite effects by transfecting anti-miR-330 precursor. [score:1]
As shown in Figure 3B, there was a significant inverse correlation between miR-330 and SH3GL2 protein level in the pre-miR-330 group versus pre-miR-con group (P<0.05), while there was no obvious difference between mock group and pre-miR-con group. [score:1]
A highly conservative miR-330 binding site at SH3GL2 3′-UTR 56–62 base position was predicted in many species, such as the H. Sapiens, the M. muculus and the R. Norvegius et al. The seed for miR-330 to SH3GL2 3′-UTR is shown in Figure 2A. [score:1]
To assess the effect of miR-330 on the cell cycle, the U87 and U251 cells were transfected with pre-miR-con and pre-miR-330. [score:1]
U87 and U251 cells were transfected with mock, pre-miR-330, anti-miR-330 and their negative control molecules for 72 h. Then, the cells were harvested and stained with Annexin V-FITC and PI according to the instruction of the manufacturer. [score:1]
To determine the levels of miR-330 in established glioblastoma cell lines, glioblastoma tissues and normal brain tissues, total RNAs were extracted from U87, U251 and U373 cells, glioblastoma tissues and normal brain tissues. [score:1]
The cell cycle distribution of the cells treated with miR-330 was examined using flow cytometry. [score:1]
MiR-330 negatively regulated SH3GL2 through binding to the 3′-UTR of SH3GL2. [score:1]
The effectiveness of miR-330 on SH3GL2 mRNA was analyzed by RT-PCR. [score:1]
Those transefected with anti-miR-330 group showed a lower proliferation rate than the anti-miR-con group (P<0.05). [score:1]
To further validate the effect of miR-330 on SH3GL2 gene, rescue experiment by siRNA on SH3GL2 in U87 cells was performed. [score:1]
Since the close relationship between miR-330 and the SH3GL2 gene, we analyzed the potential mechanism of this process according to the previous studies. [score:1]
The seed sequence of miR-330 matches 3′-UTR of SH3GL2 (in bold). [score:1]
For its mutagenesis, the sequence complementary to the binding site of miR-330 in its 3′-UTR (TGC TTT G) was replaced by GAA GCC A using the overlap PCR method. [score:1]
0046010.g006 Figure 6 Cell cycle distribution of U87 and U251 cells transfected with pre-miR-con and pre-miR-330. [score:1]
0046010.g002 Figure 2 (A) Schematic diagram of putative miR-330 binding site in the 3′-UTR of SH3GL2 in human. [score:1]
In this study, we firstly revealed the oncogenic role of miR-330 in human glioblastoma cells and its relationship with SH3GL2 gene. [score:1]
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3
[+] score: 51
In accordance with our results, miR-21, miR-100, and miR-125b were upregulated, whereas miR-455-3p and miR-378 were downregulated in chemoresistant BxPC-3. In addition, miR-330-5p could be detected by Tréhoux et al. as a tumor suppressor in PDAC in vitro and in vivo, sensitizing pancreatic cancer cells to gemcitabine [19]. [score:9]
We suggest that under acquired chemoresistance, accumulation of mutant p53 induces expression of miR-21-5p, miR-31*, miR-125b-5p, miR-210-3p, miR-330-3p, miR-378a-3p, miR-422a and miR-486-5p which in turn enhances proliferation by upregulating Bcl-2 expression in PDAC cells. [score:8]
RT-PCR validation of mostly dysregulated miRs confirmed that miR-138, miR-147b, miR-148a, miR-99a, miR-455-3p and miR-125b were significantly upregulated and miR-31-star, miR-422a, miR-330-3p, mir-330-5p and miR-378d were downregulated in PANC-1-GR cell clones vs. [score:8]
MiR-screening revealed significantly upregulated (miR-21, miR-99a, miR-100, miR-125b, miR-138, miR-210) and downregulated miRs (miR-31*, miR-330, miR-378) in chemoresistant PDAC (p<0.05). [score:7]
In MIA-PaCa-2-GR cell clones miR-125b, miR-210, miR-21, miR-100, miR-148a, miR-99a and miR-455-3p were significantly upregulated, whereas miR-330-3p, miR-330-5p, miR-486-5p, miR-422a and miR-31-star were significantly downregulated (Fig 6B). [score:7]
The role of microRNA-330-5p, significantly downregulated in both chemoresistant cell clones and highly predicted to target MRP-1 (ABCC1) needs to be confirmed by functional analysis. [score:6]
Interestingly, most of our chemoresistance-specific miRs (miR-21-5p, miR-100-5p, miR-125b-5p, miR-210-3p, miR-330-3p, miR-378a-3p, miR-486-5p) are predicted by IPA to be regulated by TP53 gene (Fig 10). [score:2]
Multidrug resistance proteins like MRP-1 (ABCC1) are highly predicted to be regulated by mt-p53, but also by miR-330-5p. [score:2]
MiR-21-5p, miR-100-5p, miR-125b-5p, miR-210-3p, miR-330-3p, miR-378a-3p, and miR-486-5p are predicted by IPA to be regulated by TP53 gene. [score:2]
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4
[+] score: 51
This study describes how p19 affects the RNA world and shows that: i) miR-342, miR-206, miR-330, miR-138 and miR-99b are upregulated by p19 but not by p19W164A mutant; ii) anti-miR-206 can restore the G2 phase in the presence of p19; iii) p19 and p21Q61L regulate their own alternative splicing; iv) miR-206 and miR-138 are differentially regulated by p19 and p21 H-Ras and v) P19G12S Costello mutants show a clear upregulation of miR-374, miR-126, miR-342, miR-330, miR-335 and let-7. These results allow us to conclude that the H-Ras G12S mutation plays an important role in miRNA expression and open up a new line of study to understand the consequences of this mutation on Costello syndrome. [score:13]
We analyzed the obtained miRNAs by the TARGETSCAN tool and observed that miR-330 may target SC-35 and many other SR proteins as well as an UsnRNP core protein, mir-342 may target SF4, and miR-206 may target p68 RNA helicase and many other SR proteins. [score:9]
These miRNAs included miR-342 and miR-330, which are already known to be upregulated by p19 overexpression (Fig.   1), miR-126 and miR-335, which significantly reduce the ability of CN34-LM1 and CN34-BoM1 cells to metastasize to the lung [23], miR-374, which is known to be associated with aggressive small cell lung cancer [26], and let-7, which targets Ras genes [27]. [score:8]
Those results showed that miR-330, miR-335 and miR-374 are statiscaly and significally overexpressed in those CS patients cells, and thus they are putative cadidates to be miRNAs overexpressed in CS patients (R. García-Cruz and K. Sol-Church, personnel communication). [score:5]
miRNA upregulation by p19 H-Ras was re-validated by RT-PCR with a specific Taqman assay for mature miR-206, miR-342, miR-138 and miR-330 and was found to increase 2-, 1.6-, 16- and 2.5-fold, respectively, upon overexpression of p19 in three independent experiments and quadruplicate analysis. [score:5]
Thus, p21 was found to upregulate miR-374, miR-126, miR-342, miR-335 and let-7 but not miR-330, and p21G12S was found to have the same effect as p21 on miR-374, miR-342 and miR-126. [score:4]
In contrast, p21G12S (column 5) was found to have no effect on miR-335 and let-7 but upregulates miR-330, whereas p21 does not. [score:4]
Candidate miRNAs were found to be miR-342, miR-206, miR-330, miR-138, and mirR-99b (Fig.   1a and 1), which vary with p19 but not with the specific p19mut overexpression. [score:3]
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5
[+] score: 37
Using a stringent cutoff of a match score between each miRNA and its mRNA targets followed by analysis for unique mRNAs per target list, we identified a total of 67 targets of miR-33, 217 targets of miR-330, 334 targets of miR-181a, and 25 targets of miR-10b (see Supplemental Material, Table 2). [score:13]
Furthermore, miR-330 has been suggested to act as a tumor suppressor by regulating apoptosis of cancer cells (Lee et al. 2009). [score:4]
We focused a detailed analysis on the four most significantly down-regulated miRNAs, as determined through microarray analysis and qRT-PCR: miR-33, miR-330, miR-181a, and miR-10b. [score:4]
qRT-PCR validated the findings of the decreased miRNA expression induced by formaldehyde exposure: FC = −1.3 for miR-330; FC = −7.4 for miR-181a; FC = −1.2 for miR-33; and FC = −1.5 for miR-10b [see Supplemental Material, Figure 1 (doi:10.1289/ehp. [score:3]
For this analysis, we used a stringent computational matching approach to identify predicted mRNA targets for miR-33, miR-330, miR-181a, and miR-10b. [score:3]
The predicted targets of miR-33, miR-330, miR-181a, and miR-10b generated a total of 40 networks [see Supplemental Material, Table 3 (doi:10.1289/ehp. [score:3]
The five most significantly differentially expressed miRNAs, as determined through microarray analysis, were miR-33 (FC = −5.5), miR-450 (FC = −3.6), miR-330 (FC = −2.4), miR-181a (FC = −2.1), and miR-10b (FC = −2.1). [score:3]
These findings suggest that miR-33, miR-330, and miR-10b may influence cellular disease state specifically related to cancer. [score:3]
Here, we further investigated the four miRNAs with the most significant formaldehyde -induced changes in expression:miR-33, miR-330, miR-181a, and miR-10b. [score:1]
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6
[+] score: 30
Other miRNAs from this paper: hsa-mir-326
Recent study indicated that miR-330-5p inhibits proliferation and migration of keratinocytes by targeting Pdia3 expression [52], and regulates tyrosinase and PDIA3 expression and suppresses cell proliferation and invasion in cutaneous malignant melanoma [48]. [score:12]
In miRDB, miRNAs with target score≥50 were selected, and in PITA, miRNAs with target score target score ΔΔG≤-10 kcal/mol were selected, then intersection was conducted in the selected miRNAs in miRDB and PITA, and miR-326 and miR-330-5p were got as the candidate miRNAs (Table S1– 2). [score:7]
Both miR-326 and miR-330-5p repressed cell growth in NPC cell lines, while over-expressed EWSAT1 in miR-326 or miR-330-5p treated cells, significantly reversed the growth -inhibitory role of miR-326/330-5p in CNE-1 and SUNE-1 cells (Fig. 4A-B). [score:5]
Oligonucleotides containing the wild-type (WT) or mutant (MT) puptative miR-330-5p or miR-326 binding sites of the 3′-untranslated regions (3′-UTR) of the CCND1 mRNA were ligated into the pMIR-REPORT luciferase reporter plasmid vector (see in http://www. [score:3]
The cells were washed with 1× PBS (pH7.4) and then transiently transfected with 100 nM NC or pcDNA3.1-CT-GFP-EWSAT1, si-EWSAT1, miR-326, miR-330-5p, or si-CCND1, using Lipofectamine™ 2000 (Invitrogen, Carlsbad, CA, USA) according to the manufacturer's instructions. [score:1]
The CNE-1 and SUNE-1 cells were seeded in 24-well culture plates at a density of 3 × 10 [5] cells per well, and the cells were then transfected with Vector, miR-326, miR-330-5p, pcDNA3.1-CT-GFP-EWSAT1, miR-326 plus pcDNA3.1-CT-GFP-EWSAT1, or miR-330-5p plus pcDNA3.1-CT-GFP-EWSAT1. [score:1]
pcDNA3.1-CT-GFP-EWSAT1 (NR_026949), si-EWSAT1, miR-326 (MIMAT0000756), miR-330-5p (MIMAT0000751), or si-CCND1 (NM_053056), were purchased from GenePharma Co. [score:1]
[1 to 20 of 7 sentences]
7
[+] score: 21
RAI2, which is a target of miR-330 and miR-331–5p, is described to be involved in development and is up-regulated in skeletal muscle side population cells. [score:7]
ID2 has been described to be induced by DUX4 [54], but is also a predicted target of miR-330, which is specifically expressed in FSHD samples These events suggest an alternative mechanism where some of these miRNAs could play a protective role during fetal development and delay the appearance of the FSHD phenotype until development and post-natal growth is finished. [score:7]
However, we identified 8 miRNAs exclusively expressed in FSHD1 samples (miR-330, miR-331-5p, miR-34a, miR-380-3p, miR-516b, miR-582-5p, miR-517* and miR-625) which could represent new biomarkers for this disease. [score:5]
We did not observed any miRNAs only detected in control samples but we identified 8 miRNAs which were only expressed in FSHD samples as compared to age-matched controls: miR-330, miR-331–5p, miR-34a, miR-380–3p, miR-516b, miR-582–5p, miR-517* and miR-625. [score:2]
[1 to 20 of 4 sentences]
8
[+] score: 20
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-29a, hsa-mir-33a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-124-3, mmu-mir-126a, mmu-mir-9-2, mmu-mir-132, mmu-mir-133a-1, mmu-mir-134, mmu-mir-138-2, mmu-mir-145a, mmu-mir-152, mmu-mir-10b, mmu-mir-181a-2, hsa-mir-192, mmu-mir-204, mmu-mir-206, hsa-mir-148a, mmu-mir-143, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-204, hsa-mir-211, hsa-mir-212, hsa-mir-181a-1, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-143, hsa-mir-145, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-134, hsa-mir-138-1, hsa-mir-206, mmu-mir-148a, mmu-mir-192, 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-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, mmu-mir-330, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-107, mmu-mir-17, mmu-mir-212, mmu-mir-181a-1, mmu-mir-33, mmu-mir-211, mmu-mir-29b-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-106b, hsa-mir-29c, hsa-mir-34b, hsa-mir-34c, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, hsa-mir-181d, hsa-mir-505, hsa-mir-590, hsa-mir-33b, hsa-mir-454, mmu-mir-505, mmu-mir-181d, mmu-mir-590, mmu-mir-1b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, mmu-mir-126b, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
Furthermore, miR-330 has been suggested to act as a tumor suppressor by regulating apoptosis of cancer cells (Lee et al., 2009). [score:4]
MicroRNA-330 acts as tumor suppressor and induces apoptosis of prostate cancer cells through E2F1 -mediated suppression of Akt phosphorylation. [score:4]
A detailed analysis was made on the four most significantly down-regulated miRNAs, namely miR-33, miR-330, miR-181a, and miR-10b, as determined through microarray analysis and qRT-PCR. [score:4]
A stringent computational matching approach was used to identify predicted mRNA targets for miR-33, miR-330, miR-181a, and miR-10b. [score:3]
These findings suggest that miR-33, miR-330, and miR-10b may influence cellular disease state, specifically related to cancer. [score:3]
In addition, miR-330 expression levels are reduced in human prostate cancer cells when compared with non-tumorigenic prostate cells (Lee et al., 2009). [score:2]
[1 to 20 of 6 sentences]
9
[+] score: 20
Based on the fold changes, qRT-PCR was performed to validate microarray results on 12 miRNAs, specifically miRNAs up-regulated in both heart and plasma (miR-660-3p, miR-665, miR-1285-3p and miR-4491), down-regulated in heart but up-regulated in plasma (miR-206 and miR-1268b), up-regulated in heart but down-regulated in plasma (miR-130-3p, miR-199a and miR-330-3p), down-regulated in both heart and plasma (miR-221-30, miR-487b-3p and miR-4288), were chosen for validation test in the plasma of 45 control and 45 CHF patients. [score:19]
As a result, 8 of the 12 selected miRNAs (miR-660-3p, miR-665, miR-1285-3p, miR-4491, miR-206, miR-1268b, miR-130-3p and miR-330-3p) were successfully validated in the second cohort. [score:1]
[1 to 20 of 2 sentences]
10
[+] score: 20
Thus miR-98, miR-323-3p, miR-330-3p, miR-376a, miR-494, miR-598 were down-regulated by UVA and UVB, while miR-191, miR-376c and miR-501-5p were up-regulated by both. [score:7]
Among the 6 down-regulated miRNAs after UVA- and UVB-irradiation (miR-98, miR-323-3p, miR-330-3p, miR-376a, miR-494, miR-598) 3 miRNAs (miR-98, miR-330-3p and miR-376a) shared the common regulator element Hox-2.3-undefined-site-2 (gggggtgggggggag) in their promoter regions. [score:5]
Interestingly, of these ten commonly regulated microRNAs miR-98, miR-191, miR-323-3p, miR-330-3p, miR-494, and miR-598 were reported to be also deregulated after ionizing radiation [29], [30], [31] and miR-376a was shown to be a regulator of apoptosis in response to arsenic trioxide treatment [32]. [score:4]
The down-regulated miRNA-set consists of miR-98, miR-323-3p, miR-330-3p, miR-376a, miR-494 and miR-598. [score:4]
[1 to 20 of 4 sentences]
11
[+] score: 17
The association between MAF and hsa-miR-330-3p in only one subgroup of the patients, in addition to the better prognosis found in the uncorrelated, genotype -modified group, calls for the gene and the miR to be studied together as possible novel therapeutic targets. [score:3]
Gene expression levels of hsa-miR-330-3p and MAF in Group 1 and Group 2.. [score:3]
In a very interesting manner, display, or lack of display of this allele in the miR promoter region did not associate with lower expression levels of hsa-miR-330-3p, as shown in Figure 3. 10.1371/journal. [score:3]
No mutations were found in these regions, neither for MAF, nor for hsa-miR-330-3p, for any of the patients. [score:2]
Interestingly, DNA sequence analyses shows allelic behavior of a specific SNP in the hsa-miR-330-3p is presented in conjunction with absent miR-gene association and with overall survival rate increasing dramatically (p-value = 1×10 [−8]). [score:1]
In Group 1, we see a highly significant correlation between miR-330-3p and MAF (R score = −0.8219). [score:1]
As shown in the above detailed example, the presence of association between MAF and hsa-miR-330-3p is linked to a decrease in overall survival rates. [score:1]
The right-hand panel in (B) also shows how hsa-miR-330-3p itself, without its use in the metric, does not provide any significant stratification. [score:1]
1003351.g002 Figure 2(A) The set of patients is assigned to different cohorts according to contribution, or lack of, to the correlation metric between MAF and hsa-miR-330-3p (text and Figure 1). [score:1]
Figure 2 provides the case of MAF and hsa-miR-330-3p as an example for classification into groups. [score:1]
[1 to 20 of 10 sentences]
12
[+] score: 15
, High Wycombe, UK) analysis of 1733 human microRNAs and validation by qRT-PCR showed microRNA-21, microRNA-99a, microRNA-100, microRNA-125b, microRNA-138, microRNA-147b, microRNA-148a, microRNA-210, microRNA-376a, and microRNA-455-3p to be significantly upregulated, whereas microRNA-31-star, microRNA-330-3p, microRNA-330-5p, microRNA-378d, microRNA-422a, and microRNA-486-5p were significantly downregulated. [score:7]
p < 0.05 indicates significance Expression of in vitro dysregulated microRNA-376a, microRNA-330-3p, microRNA-330-5p, microRNA-378d, microRNA-422a, microRNA-455-3p, and microRNA-486-5p did not differ between PDAC and control. [score:4]
p < 0.05 indicates significance Expression of in vitro dysregulated microRNA-376a, microRNA-330-3p, microRNA-330-5p, microRNA-378d, microRNA-422a, microRNA-455-3p, and microRNA-486-5p did not differ between PDAC and control. [score:4]
[1 to 20 of 3 sentences]
13
[+] score: 14
For example, miR-106b, miR-107, miR-130a, miR-34 [9], miR-93, miR-155, miR-181a, miR-21, miR-23a, miR-320a [8], miR-193b, miR-320b [13] are significantly up-regulated and miR-148a [11, 14], miR-330-5p [15], miR-373 [16] significantly down-regulated. [score:7]
Interestingly, among the miRNAs participating in the 50 most significant miRNA-mRNA interactions we can find: miR-106b, miR-93, miR-148a, miR-330-5p that could be interacting with more than 4 different targets at the same time. [score:3]
Interestingly, most of these miRNAs are coincident with those appearing in Table 1 (miR-374b, miR-148a, miR-181a, miR-373, miR-320a, miR-93, miR-106b, miR-497, miR-23a, miR-19b, miR-107, miR-15a, miR-330-5p, miR-144), indicating that, apart from being targeting many mRNAs, these miRNAs are participating in the most reliable interactions. [score:3]
These miRNA-mRNA interactions are miR-106b-LRRC55, miR-21-PDCD4, miR-148a-YWHAB, miR-93-FAM129A, miR-330-5p-GPI, miR-330-5p-BHLHE40, miR-93-LRIG1, miR-23a-LRIG1, miR-148a-ARF4, miR-106b-FAM129A, miR-148a-ACVR1, miR-148a-CTTNBP2NL. [score:1]
[1 to 20 of 4 sentences]
14
[+] score: 10
The relative expression level of each miRNA was calculated using the 2 [−ΔΔCt] method, in which each miRNA is quantified relative to the expression of one reference miRNA, chosen among hsa-miR-324-5p (ID 000539), hsa-miR-320a (ID 002277) and hsa-miR-330-3p (ID 000544) according to the target miRNA level of expression, and a calibrator sample. [score:7]
e. m. value of hsa-miR-137, hsa-miR-376c-3p, hsa-miR-203a-3p and hsa-miR-146a-5p relative expression level in two series of biological replicates from the first microfluidics arrays (five control and five FD hOE-MSCs) and the second arrays (four healthy control and four FD hOE-MSCs), respectively normalized by hsa-miR-320a (for both hsa-miR-137 and hsa-miR-376c-3p), hsa-miR-330-3p and hsa-miR-324-5p. [score:3]
[1 to 20 of 2 sentences]
15
[+] score: 9
Other miRNAs from this paper: hsa-mir-21
Siddiqui et al. demonstrated that EGCG treatment of nude mice subcutaneously implanted with 22Rv1 PCa cells inhibited tumor growth by down -regulating miRNA-21 and induced the up-regulation of miRNA-330, a tumor suppressor that induces apoptosis in PCa cells [122]. [score:9]
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16
[+] score: 9
Consistently, the 99 target genes of this motif module significantly overlap with the target genes of miR-330. [score:5]
MiR-330 induces apoptosis in prostate cancer cells through E2F1 -mediated suppression of Akt phosphorylation [42], which strongly supports the coordinate gene regulation by this motif module and miR-330. [score:4]
[1 to 20 of 2 sentences]
17
[+] score: 9
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]
To evaluate the possible involvement of these miRNAs in BAFF regulation, we first performed RT-qPCR analysis to quantify their expression in RAFLS and SScHDF treated with Poly(I:C) or IFN-γ for 6 h, 48 h and 72 h. This analysis revealed that miR-144*, miR-30d-3p, miR-340, miR-626, miR-330-3p and miR-302c* could not be detected in RAFLS and SScHDF (figure 1S). [score:2]
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18
[+] score: 8
Further data revealed that ALAS2 can be down-regulated directly by overexpression of miRNA-218, miRNA-518, and miRNA-330 (Figure 3B). [score:7]
The seven miRNAs were hsa-miR-124, miR-206, miR-218, miR-222, miR-330, miR-342, and miR-518. [score:1]
[1 to 20 of 2 sentences]
19
[+] score: 7
5′ end variations occurred at the same frequency in glioblastomas and non-tumor brain samples for both these miRNAs (Table S7); however, in the majority of the glioblastoma libraries, the miRNAs expressed from the 3p arms were under-represented while miR-30a-5p and miR-330-5p were enriched (Fig. S3B). [score:3]
Two major isoforms were observed for both miR-30a-3p and miR-330-3p. [score:1]
Two miRNAs worth noting are miR-30a and miR-330. [score:1]
We detected a number of miRNAs processed from both the 5p and 3p arms of their respective pre-miRNAs, such as miR-136, miR-151, miR-140, and miR-330 (Table S2, S3). [score:1]
The 3p miRNAs for miR-330 and miR-204 were preferentially detected in non-tumor brain tissue, while the 5p miRNAs were preferentially detected in glioblastomas (Table S7; Fig. S3B). [score:1]
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20
[+] score: 6
We can thus speculate that if role of miR-330 is to suppress AGRP expression, the presence of rs1157892 could lead to increase of AGRP synthesis and subsequent weight gain. [score:5]
This search revealed a sequence that overlaps rs1157892 and is highly complementary to human miR-330. [score:1]
[1 to 20 of 2 sentences]
21
[+] score: 6
In regards to age, we discovered that the expression levels of 14 miRNAs (miR-654-5p, miR-493*, miR-410, miR-376a*, miR-758, miR-381, miR-543, miR-539, miR-487b, miR-337-5p, miR-136*, miR-154*, miR-330-3p, and miR-421) were significantly higher in HCC up to 66 years old than in HCC over 67 years old. [score:3]
o.   fold changep-valuehsa-miR-654-5p3.880.00014hsa-miR-493*3.100.00016hsa-miR-4102.930.00029hsa-miR-376a*2.660.00072hsa-miR-7582.870.00073hsa-miR-3812.390.00094hsa-miR-5432.070.00119hsa-miR-5393.060.00124hsa-miR-487b2.020.00186hsa-miR-337-5p2.540.00195hsa-miR-136*2.790.00246hsa-miR-154*2.270.00337hsa-miR-330-3p2.440.00759 hsa-miR-421 2.45 0.01282We also identified miRNAs with expression levels that varied according to gender and age. [score:3]
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22
[+] score: 5
Other miRNAs from this paper: hsa-mir-96, hsa-mir-302b
miR-96 and miR-330 overexpressed and targeted AQP5 in lipopolysaccharide -induced rat lung damage of disseminated intravascular coagulation. [score:5]
[1 to 20 of 1 sentences]
23
[+] score: 5
Tréhoux S. Lahdaoui F. Delpu Y. Renaud F. Leteurtre E. Torrisani J. Jonckheere N. van Seuningen I. Micro -RNAs miR-29a and miR-330-5p function as tumor suppressors by targeting the MUC1 mucin in pancreatic cancer cells Biochim. [score:5]
[1 to 20 of 1 sentences]
24
[+] score: 5
The results indicated that miR-330-5p and miR-145 markedly inhibited MRP1 expression (Figure 1E). [score:5]
[1 to 20 of 1 sentences]
25
[+] score: 5
The remaining four miRNAs (miR-324-5p, miR-330-3p, miR-509 and miR-625) caused a slight reduction in the expression levels of the truncated isoform of NTRK3 (maximum 15%), but none of them reached statistical significance. [score:3]
In the case of pGL4.13-TR, the luciferase activity was significantly reduced by 8 miRNAs (Figure 1A), all of which were predicted by at least one program: miR-128, miR-324-5p, miR-330, miR-485-3p, miR-509, miR-625, miR-765 and miR-768-5p. [score:1]
Luciferase-validated miRNAs were therefore transfected into either undifferentiated (miR-128, miR-324-5p, miR-330, miR-485-3p, miR-509, miR-625, miR-765 and miR-768-5p) or differentiated SH-SY5Y cells (miR-151-3p and miR-185), and protein levels were assessed by western blotting 72 h after transfection. [score:1]
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26
[+] score: 5
In this analysis, we observed that two miRNAs – miR-499-3p and miR-330-5p – were upregulated in cancer samples and followed the enrichment, suggesting they are key miRNAs in male breast cancer. [score:4]
miR-499-3p and miR-330-5p miRNA follow the enrichment, decreasing in the gynecomastia and increasing in the male breast cancer samples. [score:1]
[1 to 20 of 2 sentences]
27
[+] score: 4
Johnson et al. [10]– [12] reported miR-29a and miR-330 to be significantly up-regulated in HD samples, neither of which was found to be altered in this study [10]. [score:4]
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28
[+] score: 4
For example, miR-330-3p regulates PDCD4 and might have an oncogenic role in esophageal squamous cell carcinoma [26], circuit of miR-31, SOX4, and EZH2 increases tumor progression in invasive esophageal carcinomas [27], and miR-10b may target KLF4 and thus promote the migration and invasion of tumorous cells [28]. [score:4]
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29
[+] score: 3
Other miRNAs from this paper: hsa-mir-212, hsa-mir-132, hsa-mir-146a, hsa-mir-155, hsa-mir-505
do) which identified miR-132/212 being able to target both IL-1α and IL-1β [IL-1α: miR-330-5p, 326, 211, 204, 488, 185, 328, 149, 299-3p, 495, 590-5p, 21, 132, 212, 340 and 144; IL-1β: miR-505, 200a, 141, 30e, a, d, c, b, 543, 181d, b, c, a, 212, 132, 24, 543, 448, 203, 136, 205, 410, 340, 374a, b, 365, 874, 150, 149, 125a-3p, 590-3p, 140-5p, 494, 194 and 653]. [score:3]
[1 to 20 of 1 sentences]
30
[+] score: 3
C) Primary study hsa-miR-330-3p:rs7252175 D) Replication study hsa-miR-1255a:rs1822168. [score:1]
A) Abdominal adipose tissue hsa-miR-1255a:rs1822168 (p-value = 1.83E-05 in primary study and p-value = 9.91E-03 in replication study) B) Abdominal adipose tissue hsa-miR-618: rs1716543 (p-value = 5.34E-04 in primary study and p-value = 5.80E-03 in replication study) C) Abdominal adipose tissue hsa-miR-146a*:rs2961920 (p-value = 5.87E-04e in primary study and p-value = 6.45E-06 in replication study) D) Gluteal adipose tissue hsa-miR-1255a:rs1822168 (p-value = 1.56E-05 in primary study and p-value = 1.65E-04 in replication study), E) Gluteal adipose tissue hsa-miR-1307:rs11191666 (p-value = 1.27E-04 in primary study and p-value = 3.55E-04 in replication study), F) Gluteal adipose tissue hsa-miR-330-3p:rs7252175 (p-value = 3.85E-04 in primary study and p-value = 4.04E-02 in replication study). [score:1]
F) Replication study hsa-miR-330-3p:rs7252175. [score:1]
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31
[+] score: 3
The mean expression of only two of the Affymetrix U133A probes was significantly different between groups (ELM2 hosting miR-330 with p = 0.03; MYH6 hosting miR-208 with p = 0.03). [score:3]
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32
[+] score: 3
In addition, they showed expression trend that were the opposite of their related miRNAs, hsa-miR-330-3P, hsa-miR-342-3P, hsa-miR-501-3P, hsa-miR-331-3P, hsa-miR-340-3P, hsa-miR-3607-3P, hsa-miR-3614-3P and hsa-miR-374a-3P. [score:3]
[1 to 20 of 1 sentences]
33
[+] score: 3
Huntington's disease exhibited the largest degree, which is associated with numerous miRNAs such as hsa-miR-128 [42], hsa-miR-9* [43], and hsa-miR-330 [44]. [score:3]
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34
[+] score: 3
In addition, miR-128, miR-134, and miR-330 targeted the MMP-3 (matrix metalloproteinase), MMP-10, and MMP-13, respectively, in a mouse mo del of chemically induced colitis -associated cancer [21]. [score:3]
[1 to 20 of 1 sentences]
35
[+] score: 3
Of these, 5 miRNAs (miR-137, miR-214-3p, miR-301a-3p, miR-330-3p and miR-383-5p) affect all four categories, linking them strongly to leukemia pathogenesis and highlighting their potential as therapeutic targets. [score:3]
[1 to 20 of 1 sentences]
36
[+] score: 3
In one study, they showed that the CD44 3′UTR serves as a competitor for hsa-miR-216a-5p, hsa-miR-330-3p, and and hsa-miR-608 to increase CD44 and CDC42 protein levels in the breast cancer cell line MT-1, resulting in inhibition of cell proliferation and tumor-formation, promotion of angiogenesis, and induction of apoptosis [39]. [score:3]
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[+] score: 3
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-31, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-199a-1, hsa-mir-208a, hsa-mir-30c-2, hsa-mir-147a, hsa-mir-10a, hsa-mir-34a, hsa-mir-181b-1, hsa-mir-199a-2, hsa-mir-203a, hsa-mir-204, hsa-mir-217, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-200b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-132, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-193a, hsa-mir-195, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, hsa-mir-30c-1, hsa-mir-219a-2, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-302d, hsa-mir-374a, hsa-mir-375, hsa-mir-378a, hsa-mir-328, hsa-mir-342, hsa-mir-325, hsa-mir-424, hsa-mir-429, hsa-mir-450a-1, hsa-mir-486-1, hsa-mir-146b, hsa-mir-497, hsa-mir-520e, hsa-mir-520f, hsa-mir-520a, hsa-mir-520b, hsa-mir-520c, hsa-mir-520d, hsa-mir-520g, hsa-mir-520h, hsa-mir-450a-2, hsa-mir-503, hsa-mir-608, hsa-mir-625, hsa-mir-629, hsa-mir-663a, hsa-mir-1271, hsa-mir-769, hsa-mir-378d-2, hsa-mir-675, hsa-mir-147b, hsa-mir-374b, hsa-mir-663b, hsa-mir-378b, hsa-mir-378c, hsa-mir-374c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-4661, hsa-mir-219b, hsa-mir-203b, hsa-mir-378j, hsa-mir-486-2
Among these, miR-328, miR-330-3p, miR-221, and miR-125a-5p had their expressions reduced, while miR-192, miR-486-5p, miR-19b, miR-106a, miR-130b, miR-18a, and miR-769-5p displayed increased levels after the intervention. [score:3]
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38
[+] score: 3
Only five miRNAs - miR-96, miR-888, miR330-3p, let-7a, and miR-146a - were significantly less abundant in CB reticulocytes compared to AB reticulocytes and were also significantly down-regulated in hemin treated K562 cells (Figure 2). [score:3]
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39
[+] score: 2
Age-related miRNAs had higher degrees than non age-related miRNAs, which indicated that age-related miRNAs (e. g. hsa-mir-130a, has-mir-330-3p and hsa-mir-29a) regulated much more mRNAs than non age-related miRNAs in the miRNA-mRNA network. [score:2]
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40
[+] 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-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-125a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-136, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-24-1, mmu-mir-191, hsa-mir-196a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-122, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-196a-2, hsa-mir-181a-1, mmu-mir-296, mmu-mir-298, mmu-mir-34c, mmu-let-7d, mmu-mir-130b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-143, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-136, hsa-mir-138-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-148a, mmu-mir-196a-1, mmu-mir-196a-2, 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-20a, mmu-mir-21a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-93, mmu-mir-34a, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-330, mmu-mir-346, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-107, mmu-mir-17, mmu-mir-19a, mmu-mir-100, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34c, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-375, hsa-mir-381, mmu-mir-375, mmu-mir-381, mmu-mir-133a-2, hsa-mir-346, hsa-mir-196b, mmu-mir-196b, hsa-mir-18b, hsa-mir-20b, hsa-mir-146b, hsa-mir-519d, hsa-mir-501, hsa-mir-503, mmu-mir-20b, mmu-mir-503, hsa-mir-92b, mmu-mir-146b, mmu-mir-669c, mmu-mir-501, mmu-mir-718, mmu-mir-18b, mmu-mir-92b, hsa-mir-298, mmu-mir-1b, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-718, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Mir-136 and mir-718 were not detectable in the adipocyte cultures using the Taqman assays-on-demand, while mir-346, mir-298, mir-330 and mir-501 were expressed at low levels (Ct levels above 33), see Table 1. This suggests that currently there is no gold standard method (when RNA is limiting) to validate miRNA data profiles. [score:2]
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[+] score: 1
miRNA Normalized Mean Values ± SD [Sample 1–Sample 2] miRNA Normalized Mean Values ± SD [Sample 1–Sample 2] let-7b-3p 4.73 ± 2.21 [6.30–3.17] miR-320b 8.93 ± 0.22 [9.08–8.77] let-7e-5p 5.24 ± 0.032 [5.22–5.27] miR-325 5.15 ± 0.72 [4.64–5.66] let-7f-5p 5.24 ± 1.49 [4.18–6.29] miR-330-3p 9.23 ± 2.37 [7.56–10.91] let-7f-2-3p 7.90 ± 0.10 [7.83–7.97] miR-337-3p 2.70 ± 1.19 [1.86–3. [score:1]
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42
[+] score: 1
Additionally, miR-202 miR-423-5p miR-503 miR-184 and miR-922 bind also to the conserved binding region chromosome 15 positions 58889443–5889473 and miR-330-5p (chr15:58889149–58889178), miR-671-5p (chr15:58889720–58889745) and miR-432 (chr15:58889688–58889718) bind to a region with good conservation also to the far related species zebra fish, but these eight miRNAs have no indication to be involved in AD (Table  1). [score:1]
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43
[+] score: 1
[*] The repressive ratio of hsa-miR-330 is inconsistent from original results. [score:1]
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44
[+] score: 1
miR-330, miR-582-5p, and miR-363 promote GSC migration and invasion by reducing apoptosis [94, 95]. [score:1]
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45
[+] score: 1
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-20a, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-93, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-23b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-101a, mmu-mir-124-3, mmu-mir-125a, mmu-mir-130a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-136, mmu-mir-138-2, mmu-mir-140, mmu-mir-144, mmu-mir-145a, mmu-mir-146a, mmu-mir-149, mmu-mir-152, mmu-mir-10b, mmu-mir-181a-2, mmu-mir-182, mmu-mir-183, mmu-mir-185, mmu-mir-24-1, mmu-mir-191, mmu-mir-193a, mmu-mir-195a, mmu-mir-200b, mmu-mir-204, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, 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-204, hsa-mir-181a-1, hsa-mir-221, hsa-mir-222, hsa-mir-200b, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-130b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-130a, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-138-2, hsa-mir-140, hsa-mir-144, hsa-mir-145, hsa-mir-152, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-136, hsa-mir-138-1, hsa-mir-146a, hsa-mir-149, hsa-mir-185, hsa-mir-193a, hsa-mir-195, hsa-mir-320a, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, 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-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-20a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-93, mmu-mir-34a, mmu-mir-330, mmu-mir-339, mmu-mir-340, mmu-mir-135b, mmu-mir-101b, hsa-mir-200c, hsa-mir-181b-2, mmu-mir-107, mmu-mir-10a, mmu-mir-17, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-320, mmu-mir-26a-2, mmu-mir-221, mmu-mir-222, mmu-mir-29b-2, mmu-mir-135a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-361, mmu-mir-361, hsa-mir-376a-1, mmu-mir-376a, hsa-mir-340, hsa-mir-135b, hsa-mir-339, hsa-mir-335, mmu-mir-335, mmu-mir-181b-2, mmu-mir-376b, mmu-mir-434, mmu-mir-467a-1, hsa-mir-376b, hsa-mir-485, hsa-mir-146b, hsa-mir-193b, hsa-mir-181d, mmu-mir-485, mmu-mir-541, hsa-mir-376a-2, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, mmu-mir-301b, mmu-mir-674, mmu-mir-146b, mmu-mir-467b, mmu-mir-669c, mmu-mir-708, mmu-mir-676, mmu-mir-181d, mmu-mir-193b, mmu-mir-467c, mmu-mir-467d, hsa-mir-541, hsa-mir-708, hsa-mir-301b, mmu-mir-467e, mmu-mir-467f, mmu-mir-467g, mmu-mir-467h, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-467a-4, mmu-mir-467a-5, mmu-mir-467a-6, mmu-mir-467a-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, hsa-mir-320e, hsa-mir-676, mmu-mir-101c, mmu-mir-195b, mmu-mir-145b, mmu-let-7j, mmu-mir-130c, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
35E-0215mmu-miR-29a-5pmir-290.297.563.17E-051.34E-036mmu-miR-30d-5pmir-300.269.683.57E-063.79E-0439mmu-miR-30e-5pmir-300.2610.871.18E-031.92E-0243mmu-miR-30e-3pmir-300.298.171.61E-032.38E-0276mmu-miR-30b-5pmir-300.2511.791.12E-029.39E-029mmu-miR-320-3pmir-3200.267.491.07E-056.88E-0471mmu-miR-330-5pmir-3300.157.709.69E-038.70E-0230mmu-miR-335-5pmir-3350.2310.514.00E-048. [score:1]
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[+] score: 1
Other miRNAs from this paper: hsa-mir-26b, hsa-mir-206
36, 37 Other miRNAs, including hsa-miR-26b-5p and hsa-miR-330-3p, are also expected to have binding sites in the 3′UTR of PFKFB3, although functional validation remains to be performed. [score:1]
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[+] score: 1
Interestingly, of the miRNAs which are known to alter the phenotype of prostate cancer cells, some are considered oncogenic (e. g., miR-221/-222, miR-21 and miR-125b), while others are considered to be tumor suppressors (e. g., miR-101, miR-126*, miR-146a, miR-330, the miR-34 cluster and miR-200 family). [score:1]
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[+] score: 1
hsa-miR-10a, hsa-miR-128, hsa-miR-1307, hsa-miR-140-3p, hsa-miR-185, hsa-miR-196a, hsa-miR-25, hsa-miR-320a, hsa-miR-330-3p, hsa-miR-340, hsa-miR-423-5p, hsa-miR-629 and hsa-miR-744 significantly associated with the mitochondria of HEK293. [score:1]
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