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17 publications mentioning mmu-mir-330

Open access articles that are associated with the species Mus musculus 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: hsa-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: 209
Other miRNAs from this paper: mmu-mir-199a-1, mmu-mir-31, mmu-mir-199a-2, mmu-mir-378b
Moreover, in this study, we demonstrated that miR-330-5p directly down-regulates the expression of SRPR by targeting its 3′ UTR, suggesting that the inhibitory effect of SRPR down-regulation on cell proliferation is mediated by miR-330-5p. [score:14]
Similar to SRPR, knockdown of Pdia3 expression by miR-330-5p inhibits proliferation of mouse keratinocytes [9], which explains why Srpr overexpression did not fully rescue the inhibitory effect of miR-330-5p on keratinocyte proliferation. [score:10]
For example, up-regulation of miR-330-5p inhibits keratinocyte proliferation and migration by targeting Pdia3 expression [9]. [score:10]
We also showed that miR-330-5p directly suppresses Srpr expression by targeting its 3′ UTR. [score:8]
3’ UTR of Srpr is a direct target of miR-330-5p in mouse keratinocyteThe web -based target prediction software programs (TargetScan and microRNA. [score:8]
In this cell line, Srpr expression was also down-regulated by miR-330-5p through direct binding to its 3′ UTR (S4 Fig). [score:7]
MiR-330-5p regulates endogenous Srpr expression in mouse keratinocyteUsing microarray analysis, we recently reported that expression of many genes was significantly changed in miR-330-5p -overexpressing PAM212 cells compared to the control [9]. [score:7]
MiR-330-5p mimic (Dharmacon) or miR-330-5p inhibitor (Dharmacon) was used for miR-330-5p over -expression or suppression, respectively. [score:7]
In addition, we performed real-time PCR to compare expression level of Srpr with those of several genes whose expressions were regulated by miR-330-5p in keratinocyte [9]. [score:6]
In particular, we found that Srpr expression was down-regulated by miR-330-5p. [score:6]
Real-time PCR was performed to compare expression level of Srpr with several genes whose expressions were regulated by miR-330-5p in keratinocyte. [score:6]
We found that transfection of miR-330-5p inhibitor led to a significant induction of the endogenous Srpr expression (Fig 3F). [score:5]
S2 Fig (A) Over -expression of miR-330-5p inhibited proliferation of PAM212 cells in a dose dependant manner. [score:5]
S1 FigComparison of Srpr expression with several genes that regulated by miR-330-5p in keratinocyte. [score:4]
To examine whether SRPR expression is directly regulated by miR-330-5p, we performed a luciferase reporter assay using constructs generated in the psiCHECK-2 dual luciferase vector. [score:4]
Using microarray analysis, we recently reported that expression of many genes was significantly changed in miR-330-5p -overexpressing PAM212 cells compared to the control [9]. [score:4]
These data indicate that SRPR expression is regulated by miR-330-5p at both mRNA and protein levels. [score:4]
Previous reports indicated that deregulated miR-330-5p expression controls cell proliferation in colorectal and prostate cancers [19, 20]. [score:4]
Therefore, miR-330-5p is a key regulator of cell cycle because it targets genes associated with this process. [score:4]
To test this hypothesis, we first validated Srpr down-regulation by miR-330-5p using real-time quantitative PCR on total RNAs that were used for microarray analysis in our previous study [9]. [score:4]
These data suggest that Srpr is a direct target of miR-330-5p. [score:4]
Finally, we used proliferation assay to investigate whether miR-330-5p inhibits keratinocyte proliferation by targeting SRPR expression. [score:4]
Srpr is a direct target of miR-330-5p in mouse keratinocyte. [score:4]
Comparison of Srpr expression with several genes that regulated by miR-330-5p in keratinocyte. [score:4]
0164896.g004 Fig 4 Srpr is a direct target of miR-330-5p in mouse keratinocyte. [score:4]
3’ UTR of Srpr is a direct target of miR-330-5p in mouse keratinocyte. [score:4]
Recently, we also showed that miR-330-5p inhibits keratinocyte proliferation by arresting cells in G0/G1 phase [9]. [score:3]
We previously showed that miR-330-5p inhibits proliferation of mouse keratinocytes [9] and have confirmed this effect in the present study (S2 Fig). [score:3]
Co-transfection with the Srpr CDS construct rescued inhibition of cell proliferation by miR-330-5p. [score:3]
These results raise a possibility that regulation of Srpr by miR-330-5p occurs in various cell types and plays important roles in regulation of cell proliferation. [score:3]
In order to confirm these findings, we also investigated the expression of Srpr using a miR-330-5p inhibitor. [score:3]
MiR-330-5p regulates Srpr expression in mouse epidermal keratinocyte. [score:3]
Expression of Srpr mRNA was consistently decreased in PAM212 cells transfected with the miR-330-5p mimic in comparison with control -transfected cells (Fig 3C). [score:3]
Next, we analyzed the effect of miR-330-5p on Srpr expression in keratinocytes at the mRNA and protein levels using real-time quantitative PCR and western blotting, respectively. [score:3]
S4 Fig Srpr is a target of miR-330 in mouse 3T3-L1 cells. [score:3]
Co-transfection with the Srpr CDS construct rescued inhibition of cell proliferation by miR-330-5p (Fig 4C–4E). [score:3]
MiR-330-5p regulates endogenous Srpr expression in mouse keratinocyte. [score:3]
Srpr is a target of miR-330 in mouse 3T3-L1 cells. [score:3]
Similarly, SRPR expression was reduced by miR-330-5p mimic treatment (Fig 3D and 3E). [score:3]
Inhibition of proliferation by miR-330-5p. [score:3]
Therefore, we conclude that SRPR mediates the inhibitory effect of miR-330-5p on mouse keratinocyte proliferation. [score:3]
These data suggest that miR-330-5p -mediated regulation of SRPR controls proliferation of epidermal keratinocytes. [score:2]
On the basis of these observations, we hypothesized that the regulation of cell proliferation by SRPR might be mediated by miR-330-5p. [score:2]
This effect of SRPR is controlled by miR-330-5p. [score:1]
In line with this finding, the 3′ UTR of Srpr mRNA contains a seed sequence for miR-330-5p, which is conserved in various species (Fig 3A). [score:1]
These findings provide evidence for a new role of SRPR and miR-330-5p in keratinocytes and, more generally, in skin biology. [score:1]
Transfection experiments were performed with Srpr siRNA or the miR-330-5p mimic using DharmaFECT 1 transfection reagent. [score:1]
org) suggested that a binding site for miR-330-5p is present in the 897–904 bp region of the Srpr 3′ UTR (Fig 4A). [score:1]
Then the construct containing the full length 3’ UTR of Srpr (+1987 bp -+2904 bp, Table 1) was transfected into cells with miR-330-5p mimic or control mimic using the Lipofectamine 2000 reagent. [score:1]
As shown in Fig 4B, the wild-type construct with full-length 3′ UTR showed significantly decreased luciferase activity when cells were co -transfected with the miR-330-5p mimic at both 50 nM and 100 nM concentrations. [score:1]
However, luciferase activity did not change significantly when cells were co -transfected with the deletion mutant lacking the miR-330-5p binding site and the miR-330-5p (Fig 4B). [score:1]
However, luciferase activity did not change significantly when cells were co -transfected with the deletion mutant lacking the miR-330-5p -binding site and the miR-330-5p. [score:1]
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3
[+] score: 209
We found that knockdown of Dicer1 expression resulted in downregulation of miR-128/miR-134/miRNA-330 and upregulation of Mmp3/Mmp10/Mmp13 (Figure 4C). [score:10]
Murine miR-128, miR-134, and miR-330 directly target and inhibit Mmp3, Mmp10, and Mmp13, respectivelyTo predict whether miRNAs target Mmp3, Mmp10, and/or Mmp13 in murine colon cancer cells, we first utilized the bioinformatics algorithms TargetScan, miRWalk, microRNA. [score:10]
Then we asked whether down-regulation of Dicer1 led to down-regulation of miR-128, miR-134 and miRNA-330, and consequently up-regulation of Mmp3/Mmp10/Mmp13 particularly? [score:10]
MiR-128, miR-134, and miR-330 suppress the tumorigenicity of murine colon cancer cells in vitro and in vivoSince miR-128, miR-134, and miR-330 can target Mmp3, Mmp10, and Mmp13, respectively and are downregulated in the inflammation-cancer link, we next explored the functions of miR-128, miR-134, and miR-330 with respect to their contributions to the tumorigenic potential of the CT26. [score:8]
Furthermore, we indicated that knockdown of Dicer1 resulted in downregulation of miR-128/miR-134/miRNA-330 and upregulation of Mmp3/Mmp10/Mmp13 (Figure 4C). [score:8]
Gapdh was used as the internal control, and the expression values of “mimics or inhibitor control” were set as 1. (D) Transfection with miR-128, miR-134, or miR-330 mimic decreased Mmp3, Mmp10, and Mmp13 protein levels, respectively, whereas transfection with the miR-128, miR-134, or miR-330 inhibitor increased Mmp3, Mmp10, and Mmp13 levels, respectively, in CT26. [score:7]
Because overexpression of miR-128, miR-134, or miR-330 could inhibit tumorigenesis in vitro, we next asked whether these miRNAs could inhibit the metastatic potential of CT26. [score:7]
Figure 5miR-128, miR-134, and miR-330 suppress the tumorigenicity of murine colon cancer cells and inhibit tube formation of endothelial cells in vitro (A) showing that miR-128, miR-134, and miR-330 suppressed the migration of CT26. [score:7]
These results provided evidence that each of miR-128, miR-134, and miR-330 directly recognizes the respective 3′-UTR of the Mmp3, Mmp10, and Mmp13 mRNAs and thereby inhibits their translation. [score:6]
Murine miR-128, miR-134, and miR-330 directly target and inhibit Mmp3, Mmp10, and Mmp13, respectively. [score:6]
Since miR-128, miR-134, and miR-330 can target Mmp3, Mmp10, and Mmp13, respectively and are downregulated in the inflammation-cancer link, we next explored the functions of miR-128, miR-134, and miR-330 with respect to their contributions to the tumorigenic potential of the CT26. [score:6]
These observations suggested that miR-128, miR-134, and miR-330 can suppress the migration, invasion, and proliferation of murine colon cancer cells in vitro and that they also can inhibit endothelial cell tube formation to some extent. [score:5]
To verify whether Mmp3, Mmp10, and Mmp13 are direct targets of miR-128, miR-134, and miR-330, respectively, we used a luciferase assay to test the binding of each miRNA to the respective gene's 3′ untranslated region (UTR). [score:5]
miR-128, miR-134, and miR-330 suppress the tumorigenicity of murine colon cancer cells and inhibit tube formation of endothelial cells in vitro. [score:5]
A total of 3761, 1020, and 1686 possible targets for miR-128, miR-134, and miR-330, respectively, were predicted by TargetScan, miRWalk, and miRanda. [score:5]
Overexpression of the miR-128, miR-134, or miR-330 mimic clearly delayed wound gap closure compared with each mimic control, whereas knockdown of miR-128, miR-134, or miR-330 using the corresponding miRNA inhibitor had the opposite effect (Figure 5A). [score:5]
We then used DAVID Resources Analysis Tools to classify the function of these target genes, revealing that most target genes of miR-128, miR-134, and miR-330 are involved in signaling pathways such as MAPK, Wnt, TGF-β, and mTOR and in the function of adherens junctions (Figure 3C), all of which are important for tumorigenesis. [score:5]
WT cells overexpressing miR-128, miR-134, or miR-330 inhibited tube formation. [score:5]
Mmp3, Mmp10, and Mmp13 are direct targets of murine miR-128, miR-134, and miR-330, respectively. [score:4]
Inflammation -dependent downregulation of miR-128, miR-134, and miR-330 during murine CAC progression and an inverse correlation with the levels of Mmp3, Mmp10, and Mmp13. [score:4]
The mechanism responsible for the downregulation of miR-128, miR-134, and miR-330 during CAC progression. [score:4]
The matrigel invasion assay showed that overexpression of the miR-128, miR-134, or miR-330 mimic inhibited the in vitro invasive potential of CT26. [score:4]
Figure 3 Mmp3, Mmp10, and Mmp13 are direct targets of murine miR-128, miR-134, and miR-330, respectively (A) Scheme for the potential binding site of miR-128, miR-134, and miR-330 in the 3′-UTR of Mmp3, Mmp10, and Mmp13 and the sequence of each intact miR-128, miR-134, and miR-330 binding site (wild-type, wt) and its mutant (Mut) within the luciferase reporter vector. [score:4]
These results suggested that murine miR-128, miR-134, and miR-330 target Mmp3, Mmp10, and Mmp13, respectively. [score:3]
Figure 3B shows that addition of in vitro transcribed miR-128, miR-134, and miR-330 mimics significantly suppressed the luciferase activity of the Mmp3, Mmp10, and Mmp13 3′-UTR upon cotransfection with the luciferase vector (wild-type, mutant, or blank control) with the in vitro transcribed miRNA (miR-128, miR-134, miR-330, or control) mimics into human embryonic kidney (HEK293) cells. [score:3]
MiR-128, miR-134, and miR-330 suppress the tumorigenicity of murine colon cancer cells in vitro and in vivo. [score:3]
MiR-128, miR-134, and miR-330 overexpression in murine colon cancer cells attenuated the ability of the cells to proliferate, migrate, and invade other tissues. [score:3]
WT and found that the miR-128, miR-134, and miR-330 mimics reduced the levels of Mmp3, Mmp10, and Mmp13 mRNAs, respectively, whereas each of the inhibitors increased Mmp3, Mmp10, and Mmp13 levels, respectively (Figure 2C). [score:3]
miR-128, miR-134, and miR-330 suppress the metastasis of murine colon cancer cells in a nude mouse xenograft mo del. [score:3]
miR-128, miR-134, and miR-330 suppressed the luciferase activity of Mmp3, Mmp10, and Mmp13, respectively, in luciferase wild-type reporter constructs. [score:3]
We next searched for possible target genes of miR-128, miR-134, and miR-330 using web -based bioinformatics algorithms. [score:3]
Furthermore, the expression levels of miR-128, miR-134, and miR-330 correlated negatively with those of Mmp3, Mmp10, and Mmp13, respectively, in a macrophage mo del of inflammation (r = –0.578, r = –0.65, r = –0.668, respectively; Figure 2E). [score:3]
WT cells with miR-128, miR-134, or miR-330 mimics resulted in decreased expression of Mmp3, Mmp10, or Mmp13, respectively, within the resulting tumors. [score:3]
These results indicated that miR-128, miR-134, and miR-330 can suppress the metastasis of murine colon cancer cells to lung. [score:3]
Transfection of cells with Mmp3, Mmp10, or Mmp13 rescued the angiogenic capabilities of cells overexpressing miR-128, miR-134, or miR-330. [score:3]
As shown in Figure 5C, overexpression of the miR-128, miR-134, or miR-330 mimic attenuated CT26. [score:3]
The functions of these miRNAs were assessed by transfecting the cells with miR-128, miR-134, and miR-330 mimics (or the corresponding chemically synthesized miRNA inhibitors). [score:3]
Further, immunohistochemical staining revealed that transfection with the miR-128, miR-134, or miR-330 mimic resulted in decreased expression of Mmp3, Mmp10, or Mmp13, respectively, within tumors (Figure 6E). [score:3]
MiR-128, miR-134, and miR-330 have been reported to play substantive roles in regulating cell proliferation, survival, motility, apoptosis, and invasion [31– 35]. [score:2]
Moreover, nude mice injected with cells overexpressing miR-128, miR-134, or miR-330 mimic had significantly fewer macroscopic lung metastases compared with the mimic controls (Figure 6D). [score:2]
We thus assessed the intracellular levels of Dicer1 and Drosha in RAW264.7 macrophages to verify whether their dysregulation played a role in the observed decrease in miR-128, miR-134, and miR-330 levels during CAC progression. [score:2]
When compared with normal colonic tissues, there was a significantly decreased expression of miR-128, miR-134, and miR-330 detected in the colorectal cancer specimens (Supplemental Figure 1B, right). [score:2]
In the present study, we identified miR-128, miR-134, and miR-330 as negative regulators of Mmp3, Mmp10, and Mmp13, respectively. [score:2]
WT cells overexpressing miR-128, miR-134, or miR-330 when compared with that of the control group cells. [score:2]
In addition, we assayed the expression levels of miR-128, miR-134, and miR-330 in human colorectal cancer and normal colonic tissues. [score:2]
WT cells that had been transfected with miR-128, miR-134, and miR-330 mimics (or mimics control) were injected into the tail vein of nude mice. [score:1]
Cells that had been transfected with an miR-128, miR-134, or miR-330 mimic or control mimic were injected into the tail vein of nude mice, and the efficiency of transfection was verified (Figure 6A). [score:1]
WT) transfected with miR-128, miR-134, or miR-330 mimics or mimics control. [score:1]
As shown in Figure 3A, two miR-128 -binding sites were identified in the 3′-UTR of Mmp3 mRNA, and likewise one miR-134 -binding site was identified for Mmp10 mRNA and one miR-330 -binding site was identified for Mmp13 mRNA. [score:1]
revealed that miR-128, miR-134, and miR-330 decreased the levels of Mmp3, Mmp10, and Mmp13, respectively (Figure 2D). [score:1]
There was perfect base pairing between the seed sequence of mature miR-128/miR-134/miR-330 and the 3′-UTR of Mmp3/Mmp10/Mmp13 mRNAs, respectively. [score:1]
All primers used are described in Supplemental Table 1. With respect to Mmp13, we directly synthesized sense and antisense strands of its 3′-UTR that contained the binding site for miRNA-330. [score:1]
To assess the effect of each miRNA (miR-128, miR-134, miR-330) on tumor metastasis, CT26. [score:1]
Thus we tested the effect of miR-128, miR-134, and miR-330 on the metastasis-related aspects in murine colon cancer cells. [score:1]
WT cells transfected with the miR-128, miR-134, and miR-330 mimics or mimics control. [score:1]
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4
[+] score: 99
Neuronal miR-326 was reported as a tumor suppressor gene in the brain (Kefas et al., 2009), while miR-330 was reported to suppress breast cancer and colorectal cancer development by targeting CDC42 (Jeyapalan et al., 2011; Li et al., 2013). [score:8]
CDC42 protein level was markedly inhibited by miR-330-5p, while miR-326-3p overexpression did not show a significantly inhibitive effect (Figure 4D). [score:7]
Rpph1, serving as an lncRNA hub in the ceRNA network targeting miR-330-5p and miR-326-3p, was found to be upregulated in APPswe/PS1ΔE9 cortexes and hippocampi. [score:6]
Our study shows that Rpph1 enhances the expression level of CDC42 and promotes dendritic spine formation by competing for endogenously expressed miR-330-5p. [score:5]
Under the condition of overexpression of miR-326-3p, p (vector/ Rpph1-WT) = 0.009, p (Rpph1-WT/ Rpph1-MUT) = 0.004, F = 13.048, while under the condition of overexpression of miR-330-5p, p (vector/ Rpph1-WT) = 0.033, p (Rpph1-WT/ Rpph1-MUT) = 0.005, F = 9.518. [score:5]
As one miRNA can target various mRNAs, we searched for the mutual protein coding mRNA targets of miR-326-3p and miR-330-5p. [score:5]
Rpph1 Modulates CDC42 Expression Level through miR-330-5pTo examine lncRNA–miRNA interactions in the ceRNA network, we predicted possible MREs in Rpph1 and identified miR-326-3p and miR-330-5p as potential targets. [score:5]
FIGURE 4Targeting the expression of Rpph1 and CDC42 by miR-326-3p and miR-330-5p. [score:5]
Both miR-330-5p and miR-326-3p were predicted to target CDC42, which is involved in the regulation of the actin cytoskeleton pathway. [score:4]
MicroRNA-330 acts as tumor suppressor and induces apoptosis of prostate cancer cells through E2F1 -mediated suppression of Akt phosphorylation. [score:4]
Taken together, we now show that Rpph1 competes with endogenous miR-330-5p and subsequently upregulates CDC42 to modulate actin dynamics in primarily cultured pyramidal hippocampal neurons. [score:4]
miR-330 regulates the proliferation of colorectal cancer cells by targeting CDC42. [score:4]
To confirm that miR-326-3p and miR-330-5p target CDC42 in the neural system, we transfected miRNA mimics and negative controls into Neuro-2a cells and examined the levels of CDC42 mRNA and protein. [score:3]
Rpph1 Modulates CDC42 Expression Level through miR-330-5p. [score:3]
MiR-330-5p also induces downregulation of CDC42. [score:3]
These results suggest that Rpph1 promotes the expression of CDC42 by impeding miR-330-5p binding. [score:3]
from showed that both miR-326-3p and miR-330-5p inhibit Rpph1 WT luminescence activity by 20%. [score:3]
Cdc42 mRNA levels were decreased by overexpression of miR-330-5p and miR-326-3p to 37.2 and 20%, respectively (Figure 4C). [score:3]
To examine lncRNA–miRNA interactions in the ceRNA network, we predicted possible MREs in Rpph1 and identified miR-326-3p and miR-330-5p as potential targets. [score:3]
It is noteworthy that the expression levels of both miR-326-3p and miR-330-5p did not change significantly compared to our previous microRNA-seq study (Luo et al., 2014). [score:2]
Both miR-326-3p and miR-330-5p directly bind to Rpph1. [score:2]
Relative CDC42 mRNA (C) or protein (D) levels in the Neuro-2a cell line following overexpression of miR-326-3p or miR-330-5p mimic compared to the negative control. [score:2]
MiR-330-5p has been reported to target CDC42 in human breast cancer cell line MT-1 (Jeyapalan et al., 2011) and colorectal cancer cell SW1116 (Li et al., 2013). [score:2]
Given the hypothesis that the more MREs a RNA has the more important role it may play in the ceRNA network, we further studied Rpph1, which was predicted to interact with both miR-326-3p and miR-330-5p. [score:1]
For the transfection of miR-326-3p, miR-330-3p, pcDNA-Rpph1-wt and pcDNA-Rpph1-mutant into Neuro-2a cells, 4 × 10 [5] cells were seeded in a 35-mm dish. [score:1]
To this end, we further pursued the interaction between Rpph1, miR-326-3p/miR-330-5p and CDC42. [score:1]
MiR-330-5p shares eight nucleotide binding sequences with Rpph1 while miR-326-3p shares seven nucleotide binding sequences (Figure 4A). [score:1]
We propose that one of our tested ceRNA pathways, Rpph1/miR-330-5p/CDC42, may be involved in the compensatory behavior of the brain neurons to combat synaptic loss during AD pathogenesis. [score:1]
These results suggest that miR-326-3p and miR-330-5p bind to Rpph1. [score:1]
MiR-326-3p and miR-330-3p mimics were purchased from RiboBio, Co. [score:1]
MREs of miR-326-3p (5′-CCCAGAG-3′) and miR-330-3p (5′-CCCAGAGA-3′) on Rpph1 were mutated into 5′-GCACAGAC-3′. [score:1]
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5
[+] score: 26
Other miRNAs from this paper: mmu-mir-19b-2, mmu-mir-15a, mmu-mir-16-1, mmu-mir-19b-1
The ability of GT and Q in combination with Doc to upregulate the expression of miR-15a and miR-330 and to balance miR-19b expression may partly contribute to the tumor inhibitory effect of the mixture in the present study. [score:10]
The downregulation of the tumor suppressor miR-15a and miR-330 has been wi dely found in prostate tumors compared to normal tissues particularly in more advanced tumors, associated with tumor cell survival, proliferation and invasion [34, 35]. [score:5]
The miR-330 has been shown to induce apoptosis possibly by targeting E2F1 and inhibit cell motility in PC-3 cells [35, 36]. [score:5]
The mixture significantly elevated the levels of tumor suppressor mir15a and mir330 in tumor tissues. [score:3]
Similarly, the mixture of all three chemicals significantly increased miR-330 expression compared to other treatments. [score:2]
To investigate whether miRNAs are responsive to the combination treatment of GT, Q and Doc, we selected three candidate miRNAs that have been shown to be involved in prostate cancer, including two tumor suppressor miR-15a and miR-330 and an oncomiR miR-19b. [score:1]
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6
[+] 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, 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, hsa-mir-330, 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]
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7
[+] score: 17
The up-regulation of Pmp22 and Mpz proteins in the spinal cord of MLC/SOD1 [G93A] paralleled that of mRNA expression and supports the evidence that these factors are molecular targets of microRNAs, such as miR-1, miR-9, miR-133, and miR-330, that resulted differently modulated in the spinal cord of MLC/SOD1 [G93A] mice compared to wild type littermates. [score:7]
In particular, we found down regulation of mir-1, mir-330, mir-29, mir-133, and mir-9 family members, whose dysregulation can have profound effects on neuronal physiology and pathology, including Huntington, Alzheimer, and Parkinson diseases (Saito and Saito, 2012). [score:5]
Graphs indicate relative expression of (A) mir-133a (B) mir-133b (C) mir-9 (D) mir-29 (E) mir-330 (F) mir-1. White bar refers to wild type (Wt) and black bar to MLC/SOD1 [G93A] (Tg). [score:3]
Of note, the miRnome profiling revealed the down regulation of mir-330, mir-133, and mir-1, which are involved in denervation and reinnervation processes (Jeng et al., 2009; Tsutsumi et al., 2014). [score:2]
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8
[+] score: 7
Of these miRNAs, the relatively prominent upregulated miRNAs were hsa-miR-3656, hsa-miR-139-5p, hsa-miR-4796-5p, hsa-miR-330-5p, hsa-miR-4698, hsa-miR-3124-5p, hsv2-miR-H10, hsa-miR-133b, hsa-miR-515-3p, hsa-miR-516a-5p, hsa-miR-4762-5p, hsa-miR-4508, hsa-miR-27a-5p, hsa-miR-3120-5p, hsa-miR-133a, and hsa-miR-205-5p (>15-fold), and the relatively prominent downregulated miRNAs were hsa-miR-411-3p, hsa-miR-19b-3p, hsa-miR-152, and hsa-miR-142-5p (>15-fold). [score:7]
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[+] 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]
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[+] score: 3
Other miRNAs from this paper: mmu-mir-30a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-132, mmu-mir-134, mmu-mir-135a-1, mmu-mir-138-2, mmu-mir-142a, mmu-mir-150, mmu-mir-154, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-194-1, mmu-mir-200b, mmu-mir-122, mmu-mir-296, mmu-mir-21a, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-96, rno-mir-322-1, mmu-mir-322, rno-mir-330, rno-mir-339, mmu-mir-339, rno-mir-342, mmu-mir-342, rno-mir-135b, mmu-mir-135b, mmu-mir-19a, mmu-mir-100, mmu-mir-139, mmu-mir-212, mmu-mir-181a-1, mmu-mir-214, mmu-mir-224, mmu-mir-135a-2, mmu-mir-92a-1, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-125b-1, mmu-mir-194-2, mmu-mir-377, mmu-mir-383, mmu-mir-181b-2, rno-mir-19a, rno-mir-21, rno-mir-24-1, rno-mir-27a, rno-mir-30a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-96, rno-mir-100, rno-mir-101a, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-132, rno-mir-134, rno-mir-135a, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-150, rno-mir-154, rno-mir-181b-1, rno-mir-181b-2, rno-mir-183, rno-mir-194-1, rno-mir-194-2, rno-mir-200b, rno-mir-212, rno-mir-181a-1, rno-mir-214, rno-mir-296, mmu-mir-376b, mmu-mir-370, mmu-mir-433, rno-mir-433, mmu-mir-466a, rno-mir-383, rno-mir-224, mmu-mir-483, rno-mir-483, rno-mir-370, rno-mir-377, mmu-mir-542, rno-mir-542-1, mmu-mir-494, mmu-mir-20b, mmu-mir-503, rno-mir-494, rno-mir-376b, rno-mir-20b, rno-mir-503-1, mmu-mir-1224, mmu-mir-551b, mmu-mir-672, mmu-mir-455, mmu-mir-490, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-504, mmu-mir-466d, mmu-mir-872, mmu-mir-877, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-872, rno-mir-877, rno-mir-182, rno-mir-455, rno-mir-672, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, rno-mir-551b, rno-mir-490, rno-mir-1224, rno-mir-504, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, rno-mir-466d, mmu-mir-466q, mmu-mir-21b, mmu-mir-21c, mmu-mir-142b, mmu-mir-466c-3, rno-mir-322-2, rno-mir-503-2, rno-mir-466b-3, rno-mir-466b-4, rno-mir-542-2, rno-mir-542-3
StAR may be a target gene of miR-376b, miR-150, miR-330 and miR-138. [score:3]
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[+] score: 3
In contrast, mir-29a and mir-330 expression is significantly higher in HD samples. [score:3]
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[+] 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-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, hsa-mir-330, 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
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-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-330, 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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Several of these miRNAs (mir-299, mir-431, mir-467c, mir-222, mir-32, mir-330, mir-384, mir-665, and mir-671) have previously been identified as sex-biased in the neonatal mouse whole brain and/or rat cortex [23, 48]. [score:1]
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For instance, we identified 5 hub TFs/genes (Rel, Ppp1r9a, Smad7, Ndn, and Cdkn1c) and 10 hub miRNAs (mir-92a-3p, mir-377-3p, mir-17-5p, mir-96-5p, mir-875-3p, mir-875-5p, mir-721, mir-330-3p, mir-20a-5p, and mir-19a-3p) for the monocyte lineage (Figure E in S1 File). [score:1]
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Other miRNAs from this paper: mmu-mir-122
A previous study demonstrated that one of our tested ceRNA pathways, RPPH1/miR-330-5p/CDC42, may be involved in the compensatory behaviour of brain neurons to combat synaptic loss during AD pathogenesis [18]. [score:1]
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The bar charts on the right show the read counts of 2 miRNAs (miR-487b and miR-330-5p) as examples. [score:1]
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