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28 publications mentioning hsa-mir-488

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-488. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 347
Figure 6 (A) miR-488 mimic inhibited mRNA expression of Six1 while miR-488 inhibitor upregulated the mRNA expression of Six1. [score:12]
miR-488 is downregulated in gastric cancers and functions as a tumor suppressor by targeting PAX6 expression [15]. [score:10]
In conclusion, this study demonstrated that miR-488 targets and downregulates Six1 and subsequently inhibits Drp1 signaling to regulate mitochondrial function and chemoresistance. [score:9]
miR-488 mimic upregulated miR-488 level in S KOV3 cell line and its inhibitor downregulated miR-488 level in OVCAR3 cell line. [score:9]
miR-488 mimic downregulated membrane potential while miR-488 inhibitor upregulated membrane potential. [score:9]
miR-488 mimic decreased cyclin D1, cyclin E protein expression while miR-488 inhibitor upregulated cyclin D1 and cyclin E (Figure 5). [score:8]
We found that miR-488 mimic downregulated Six1 while miR-488 inhibitor increased Six1 expression at both protein and mRNA levels (p<0.05) (Figures 5&6A). [score:8]
TargetScan software was used to predict potential miR-488 target and Six1 was on the target list. [score:7]
While miR-488 inhibitor downregulated apoptosis rate in OVCAR3 cells treated with 24 hours of cisplatin (10μM) and paclitaxel (5μM) (p<0.05). [score:6]
cyclin D1, cyclin E, p-Drp1, Drp1, Fis1 and Six1 of OVCAR3 cells were upregulated after transfection of miR-488 inhibitor. [score:6]
While in OVCAR3 cells with miR-488 inhibitor, the percentage of red fluorescence was upregulated. [score:6]
miR-488 inhibitor showed the opposite effect by upregulating cell viability. [score:6]
By using CCK8, we found that miR-488 mimic downregulated ovarian cancer proliferation rate while miR-488 inhibitor accelerated ovarian cancer proliferation (p<0.05) (Figure 2B). [score:6]
miR-488 inhibitor downregulated apoptosis in OVCAR3 cells. [score:6]
miR-488 targets and downregulates Six1 in ovarian cancer cells. [score:6]
While miR-488 inhibitor conferred cisplatin and paclitaxel resistance by upregulating OVCAR3 cell viability (p<0.05). [score:6]
We discovered that miR-488 mimic downregulated the protein levels of p-Drp1, Drp1 and Fis1, while miR-488 inhibitor showed the opposite effect on these proteins (Figure 5). [score:6]
Taken together, our data demonstrated miR-488 inhibits chemoresistance in ovarian cancer through downregulation of Six1. [score:6]
We did not found significant changes in cells transfected with mutant vector, indicating miR-488 binds to Six1 3′-UTR and suppresses its expression. [score:5]
Colony formation assay showed that miR-488 mimic downregulated colony number while miR-488 inhibitor increased colony number (p<0.05) (Figure 2C). [score:5]
We screened and examined potential targets of miR-488 using TargetScan 7.0. [score:5]
miR-488 was reported to function as a tumor suppressor in human prostate and gastric cancer by targeting androgen receptor and PAX6 [13, 15]. [score:5]
CCK8 assay demonstrated that Six1 overexpression also restored cisplatin resistance which was downregulated by miR-488 (Figure 8B). [score:5]
miR-488 inhibits proliferation and induces apoptosis by targeting androgen receptor in prostate cancer [13]. [score:5]
We found that S KOV3 has lowest miR-488 expression and OVCAR3 has the highest miR-488 expression. [score:5]
Six1 plasmid restored Drp1 and p-Drp1 status downregulated by miR-488. [score:4]
miR-488 mimic downregulated reporter activity in S KOV3 cells after transfection of wild-type vector (p<0.05) (Figure 6B). [score:4]
These data indicate that miR-488 negatively regulates ovarian cancer growth through inhibition of cell cycle transition. [score:4]
As shown in Figure 3B, miR-488 mimic transfection significant upregulated apoptosis rate in S KOV3 cells treated with 24 hours of cisplatin (10μM) and paclitaxel (5μM) (p<0.05). [score:4]
Figure 3 (A) miR-488 mimic significantly downregulated S KOV3 cell viability at 48 hours of cisplatin and paclitaxel treatment. [score:4]
Six1 is a direct target of miR-488 in ovarian cancer cells. [score:4]
When transfected with wild-type reporter, cells showed a downregulated luciferase activity with miR-488 mimic. [score:4]
Our results showed that miR-488 significantly reduced cisplatin and paclitaxel resistance, with upregulated apoptosis rate. [score:4]
To confirm the involvement of Six1 in miR-488 mediated regulation of Drp1 signaling, we overexpressed Six1 in S KOV3 cells treated with miR-488 mimic. [score:4]
Our results showed that miR-488 induced mitochondrial fusion, with downregulation of p-Drp1 and Fis1. [score:4]
miR-488 is downregulated in ovarian cancers. [score:4]
Our data showed that miR-488 expression was lower in ovarian cancer tissues compared with normal tissues, which was in accord with previous reports, indicating miR-488 is a potential tumor suppressor in ovarian cancers [15, 21]. [score:4]
We found miR-488 downregulation in 11 out of 27 serous ovarian carcinoma tissues. [score:4]
miR-488 in cancer tissues/mean miR-488 value in normal tissues <2 was regarded as significant miR-488 downregulation. [score:4]
miR-488 inhibitor lead to mitochondrial fission in OVCAR3 cells. [score:3]
We found that miR-488 mimic reduced membrane potential while its inhibitor maintained membrane potential. [score:3]
However, in Six1 overexpressed cells, the effects of miR-488 mimic on p-Drp1, Drp1 and Fis1 were not significant. [score:3]
CCK8 and colony formation assay showed that miR-488 downregulated cell growth rate and colony formation ability. [score:3]
To further validate the role of Six1 in miR-488 induced chemosensitivity, we adopted Six1 plasmid to restore its expression in miR-488 treated S KOV3 cells. [score:3]
Figure 8 (A) revealed that miR-488 mimic could inhibited p-Drp1 and Drp1. [score:3]
Nevertheless, expression pattern and roles of miR-488 in human ovarian cancer remains unclear. [score:3]
In this study, we examined miR-488 expression in paired ovarian cancer tissues using realtime PCR. [score:3]
While in OVCAR3 cells transfected with miR-488 inhibitor, mitochondria developed to fission with shorter mitochondrial shape (p<0.05) (Figure 4A). [score:3]
Mean miR-488 expression in ovarian cancers was lower than that in normal ovarian tissues (Student's t test, p<0.05) (Figure 1A&1B). [score:3]
miR-488 targets ZIP8 in osteoarthritis which reduced cartilage degradation [14]. [score:3]
miR-488 mimic inhibited cell viability in S KOV3 cells after 24 and 48 hours of treatment with cisplatin (10μM) and paclitaxel (5μM). [score:3]
Transfection of miR-488 mimic and inhibitor was performed in S KOV3 and OVCAR3 cell lines respectively. [score:3]
Real-time PCR was used to examine the expression of miR-488 in three ovarian cancer cell lines including SW626, S KOV3 and OVCAR3. [score:3]
miR-488 participates in the process of several human diseases such as peritoneal fibrosis and panic disorder [11, 12]. [score:3]
miR-488 inhibitor increased colony number of OVCAR3 cells. [score:3]
In Six1 overexpressed cells, treatment with miR-488 mimic failed to reduce p-Drp1, Drp1 and Fis1 levels. [score:3]
Expression pattern of miR-488 in ovarian cancer tissue samples. [score:3]
miR-488 inhibits cell proliferation in ovarian cancer cells. [score:3]
Since miR-488 regulates mitochondrial function and dynamics, we examined change of mitochondrial regulators including p-Drp1, Drp1 and Fis1. [score:3]
Figure 2 (A) Expression level of miR-488 in three ovarian cancer cell lines (SW626, S KOV3 and OVCAR3). [score:3]
Annexin V/PI staining showed that Six1 overexpression abrogate the apoptosis inducing effect of miR-488 (Figure 8C). [score:3]
We examined miR-488 expression in 27 pair of serous ovarian carcinoma tissues with adjacent normal ovarian tissues. [score:3]
revealed that miR-488 mimic could inhibited p-Drp1, Fis1 and Drp1. [score:3]
miR-488 mimic/miR-488 inhibitor and corresponding controls were obtained from RiboBio (Guangzhou, China). [score:3]
These data demonstrated that miR-488 could inhibit multi-drug resistance in ovarian cancers. [score:3]
Figure 1 (A) Relative expression level of miR-488 in 27 cases of fresh ovarian cancer tissues and paired normal tissues. [score:3]
Six1 overexpression also restored p-Drp1, Drp1 and Fis1 levels which were downregualted by miR-488 (Figure 8A). [score:3]
These data indicated that miR-488 is a negative regulator of mitochondrial membrane potential. [score:2]
Loss of membrane potential triggers mitochondrial apoptosis pathway through elevated mitochondrial membrane permeability and release of cytochrome c. Thus our data identified miR-488 as a negative regulator of mitochondrial function, which reduces resistance to mitochondrial apoptosis in ovarian cancer cells. [score:2]
Our data demonstrated that miR-488 is a negative regulator of Six1 mRNA and protein. [score:2]
miR-488 dysregulation is also involved in carcinogenesis. [score:2]
miR-488 regulates mitochondrial dynamics and membrane potential. [score:2]
Then we assessed if miR-488 was able to control mitochondrial apoptosis by regulating mitochondrial membrane potential. [score:2]
miR-488 regulates cell cycle proteins and Drp1 signaling. [score:2]
So we checked if miR-488 was able to regulate mitochondrial apoptosis by changing mitochondrial function, which includes mitochondrial dynamics and mitochondrial membrane potential. [score:2]
miR-488 regulates cell cycle proteins and Drp1 phosphorylation. [score:2]
miR-488 regulates Drp1 signaling and chemoresistance through Six1. [score:2]
miR-488 reduces chemoresistance to cisplatin and paclitaxel. [score:1]
Mitochondrial shape were prone to fusion after miR-488 mimic in S KOV3 cells. [score:1]
Six1 restores Drp1 signaling which is reduced by miR-488. [score:1]
To find out if miR-488 is involved in the mitochondrial dynamic balance, we checked mitochondrial morphology. [score:1]
miR-488 reduces chemoresistance in ovarian cancer cells. [score:1]
Six1 also restored chemoresistance in ovarian cancer cells, which was reduced by miR-488 mimic. [score:1]
In addition, we found a negative correlation between miR-488 and Six1 mRNA in ovarian cancer tissues, which further strengthen the link between them. [score:1]
We also used mutant miR-488 binding site C AAACA. [score:1]
These data together demonstrated that Six1 plays a central role in miR-488 induced change of chemosensitivity and mitochondrial function. [score:1]
We use luciferase reporter vector to validate the association between miR-488 and Six1. [score:1]
Next we checked the role of miR-488 on drug resistance and apoptosis. [score:1]
To date, clinical significance of miR-488 and its biological function in ovarian cancers have not been explored. [score:1]
Mitochondria in cells with miR-488 mimic was more prone to fusion with elongated mitochondrial shape in S KOV3 cells. [score:1]
displayed that cyclin D1, cyclin E, p-Drp1, Drp1, Fis1 and Six1 of S KOV3 cells were decreased with miR-488 mimic treatment. [score:1]
A negative association was found between miR-488 and Six1 (Linear regression mo del, p<0.05, Figure 1C). [score:1]
Furthermore, we checked the association between miR-488 and Six1 mRNA in 27 cases of serous ovarian cancers. [score:1]
We adopted luciferase reporter vector with wild-type miR-488 binding site at Six1 3′-UTR CUUUCA (2119-2125 of Six1 3′ UTR). [score:1]
Figure 5 displayed that cyclin D1, cyclin E, p-Drp1, Drp1, Fis1 and Six1 of S KOV3 cells were decreased with miR-488 mimic treatment. [score:1]
These data indicated that Six1 might serve as the mediator of miR-488 induced chemosensitivity. [score:1]
Effects of miR-488 on cell proliferation and invasion in ovarian cancer. [score:1]
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[+] score: 66
Furthermore, exposure of cells to IL-1β, a factor induced degeneration of articular chondrocytes [24] as confirmed by suppression of type II collagen level, down-regulated miR-488 level whereas exposure of cells to TGF-β3, a factor induced differentiation/proliferation of articular chondrocytes [25, 26] as confirmed by stimulation of type II collagen level, up-regulated miR-488 level (Figure  2B). [score:9]
Target validation study showed that miR-488 targets ZIP8 and suppression of ZIP8 in OA animal mo del showed the reduced cartilage degradation. [score:7]
Among miRNA analyzed, miR-23b, miR-30d, miR-132, miR-140-3p, miR-145, miR-150, miR-204 were up-regulated in OA chondrocytes whereas miR-22, miR-25, miR-26, miR-30c, miR-92b, miR-127, miR-194, miR-197, miR-296-5p, miR-342-3p, miR-488 were down-regulated in OA chondrocytes (Figure  1B). [score:7]
miR-488 acts as a positive role for chondrocyte differentiation/cartilage development by inhibiting MMP-13 activity through targeting ZIP-8. Osteoarthritis (OA) is the most common musculoskeletal disorder and the most prevalent articular pathology induced by multiple factors such as obesity, anatomic abnormalities, joint instability, and joint injury [1, 2]. [score:6]
In sum, our data suggest that miR-488 act as a protective role for chondrocyte differentiation/cartilage development by inhibiting MMP-13 activity through targeting ZIP-8. The authors declare that they have no competing interests. [score:6]
However, the expression of miR-488 in normal human tissues and disease states has not been extensively studied. [score:5]
In this study, miR-488 did not directly bind to 3’ UTR of MMP-13 in articular chondrocytes (data not shown) suggesting indirect regulation of MMP-13 by miR-488. [score:4]
Among ZIP-2, -7, -8 whose inductions were reversely regulated by IL-1β and TGF-β3, increased level of ZIP-8 by IL-1β inhibited with co-introduction of miR-488. [score:4]
Most significant degeneration was occurred with co-induction of miR-488 inhibitor. [score:3]
Among miRNAs tested, miR-488 was significantly decreased in OA chondrocytes Furthermore, we found that exposure of IL-1β was also suppressed whereas exposure of TGF-β3 induced the induction of miR-488 in human articular chondrocytes isolated from biopsy samples of normal cartilages. [score:3]
And most significant increase in ZIP-8 induction was occurred when cells were exposed to miR-488 inhibitor with IL-1β (Figure  3C). [score:3]
To better understand the mechanism in OA pathogenesis and investigate its effective target, we analyzed miRNA profiles during OA pathogenesis and verify the role and its functional targets of miR-488. [score:3]
Figure 3 MiR-488 targets ZIP8. [score:2]
To validate the role of miR-488 in human articular chondrocytes, chondrocytes isolated from biopsy cartilage of normal patients were treated with IL-1β. [score:1]
We next asked if the observed induction of MMP-13 activity by IL-1β is due to the modulation and interaction of miR488 to ZIP. [score:1]
The hsa-miR-488 and Negative Control lentivirus was transfected with 3rd generation packaging mix from Applied Biological Materials Inc. [score:1]
Since Zn [2+] is required for catalytic activity of MMP-13 [32], we next asked if miR-488 create the local environment for MMP-13 activation through modulation of Zn [2+] concentration. [score:1]
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[+] score: 45
Similarly, at E17.5 in Pkd1 [-/- ]animals, the up-regulation of Fgfr3 and Fgf10 (components of MAPK signaling) and down-regulation of their target miRNAs- miR-488 and miR-126-5p respectively, may stimulate MAPK signaling and cell proliferation in Pkd1 [-/- ]samples. [score:9]
Similarly, down-regulation of miR-10a, miR-126-5p, miR-204, and miR-488 at E17.5 were inversely correlated with up-regulation of Ltbp1, Edil3, P2rx7, and Fgfr3 respectively (Additional file 21). [score:7]
miR-204 and miR-488 (A) were down-regulated in Pkd1 [-/- ]kidneys whereas miR10a, miR-30a, miR-96, miR-126-5p, miR-182, miR-200a and miR-429 (B) were up-regulated in Pkd1 [-/- ]kidneys. [score:7]
Among the 9 miRNAs tested at E14.5, only two miRNAs, miR-488 and miR-204, were down-regulated in Pkd1 [-/- ]kidneys compared to WT, miR-96 did not change, and the remaining 6 miRNAs were up-regulated in Pkd1 [-/- ]kidneys compared to WT (Figure 7). [score:5]
For example, miR-30a-5p may be involved in histone deactylase inhibitor pathways, apoptosis, calcium and Wnt signaling (Figure 9); miR-10a may be involved in TGF-β and hedgehog signaling; miR-204 may be involved in calcium signaling while miR-488 may be involved in MAPK signaling by targeting Fgfr3 (Figure 9). [score:5]
Expression of 9 miRNAs (miR-204, miR-488, miR10a, miR-30a, miR-96, miR-126-5p, miR-182, miR-200a and miR-429), predicted to target significantly regulated genes at E14.5 was assayed using miRNA-qPCR. [score:5]
Expression of 9 miRNAs (miR-10a, miR-126-5p, miR-200a, miR-204, miR-429, miR-488, miR-96, miR-182 and miR-30a-5p), predicted to target significantly regulated genes at E17.5 was evaluated using miRNA-qPCR assays. [score:3]
We tested this hypothesis by determining the differential expression of 9 miRNAs (mmu-miR-10a, mmu-miR-30a-5p, mmu-miR-96, mmu-miR-126-5p, mmu-miR-182, mmu-miR-200a, mmu-miR-204, mmu-miR-429, and mmu-miR-488) between WT and Pkd1 [-/- ]genotypes at E14.5 and E17.5 (Figures 7 and 8). [score:3]
We observed that miRNAs: miRs-10a, -30a-5p, -96, -126-5p, -182, -200a, -204, -429, and -488; and the such as miR-126-5p-Fgf10, miR-488-Fgfr3, miR-182-Hdac9, miR-204-P2rx7 and miR-96-Sox6 (as shown in Table 6) have not been previously reported in ADPKD. [score:1]
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[+] score: 39
Androgen receptor is a direct target of miR-488, as miR-488 has a binding site at the 3'UTR of AR gene where it binds and suppresses its expression [75]. [score:8]
miR-488 Tumor suppressor Inhibits Androgen Receptor -mediated cell growthSikand 2010 [75] Both of these miRNAs work as tumor suppressors mediated through deregulation of multiple oncogenes, and these oncogenes include: BCL2, MCL1, CCND1, and WNT3A [25]. [score:8]
These results suggest that miR-488 could function as a tumor growth suppressor, which is mediated by deregulation of AR expression [75]. [score:6]
In both the cell lines, treatment with miR-488 mimics was found to retard the growth of these cells, but this was not the fact with AR -negative DU145 cells [75], suggesting the regulatory role of miR-488 on AR expression. [score:4]
Although it is still too premature to make conclusions, the results of these studies clearly showed that miR-488* transfection into LNCaP and C4-2B cells led to the repression of AR expression, thereby suggesting that finding a way to increase the levels of endogenous miR-488* could have a great impact on designing novel treatment strategies for PCa. [score:3]
It was shown that cells transfected with miR-488 results in reduced expression of AR in both Androgen -dependent (LNCaP) and Androgen-independent (C4-2B) PCa cells. [score:3]
Two mature molecules results from the processing of its precursors: miR-488* and miR-488 and both of them are expressed predominantly in human brain tissue [75]. [score:3]
The importance of miRNA-488. [score:1]
Studies have shown that miR-488* was not expressed in several prostate cancer cell lines, although the etiology is still unclear and thus it is currently being further investigated [75]. [score:1]
The miR-488 is encoded through AsTN1 gene. [score:1]
Another miRNA that has been associated with PCa is miR-488. [score:1]
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5
[+] score: 14
Other predictions, based on our dataset are: hsa-mir-488 – very probably involved in apoptosis (2 of 3 occurrences, 1 of them in Alu insertion) hsa-mir-526b* - very probably involved in cell adhesion (2 of 3 occurrences) hsa-mir-453 and hsa-mir-17-3p (Alu-related) and hsa-mir-22 and -302b (not related to Alus) – are probably involved in transport hsa-mir-17-3p, -412 and -453 – very probably targeting receptors (additional support: MiRanda-predicted target for hsa-mir-453 – neuron derived orphan receptor 1) hsa-mir-422a – probably targeting structural proteins. [score:7]
Other predictions, based on our dataset are: hsa-mir-488 – very probably involved in apoptosis (2 of 3 occurrences, 1 of them in Alu insertion) hsa-mir-526b* - very probably involved in cell adhesion (2 of 3 occurrences) hsa-mir-453 and hsa-mir-17-3p (Alu-related) and hsa-mir-22 and -302b (not related to Alus) – are probably involved in transport hsa-mir-17-3p, -412 and -453 – very probably targeting receptors (additional support: MiRanda-predicted target for hsa-mir-453 – neuron derived orphan receptor 1) hsa-mir-422a – probably targeting structural proteins. [score:7]
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[+] score: 12
In addition, miRNAs are possible targets for therapeutic intervention in OA, where their functions can be modulated by virtue of biotechnology advances, as depicted in Figure 2. Inflammation and cartilage erosion in OA are linked by a miRNA-488-regulated Zn [2+/]ZIP8/MTF1 pathway, which affects the expression of MMPs-ADAMTS5. [score:6]
miRNA-488 is a TGF-β3-inducible miRNA, of which expression is decreased in OA chondrocytes compared to normal chondrocytes, and that targets ZIP8 (SLC39A8), a Zn [2+] importer. [score:4]
Song J. Kim D. Lee C. H. Lee M. S. Chun C. H. Jin E. J. MicroRNA-488 regulates zinc transporter SLC39A8/ZIP8 during pathogenesis of osteoarthritis J. Biomed. [score:1]
Hence, the miRNA-488/ZIP8/MTF1/MMPs-ADAMTS5 axis is critical for the pathogenesis of OA. [score:1]
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[+] score: 12
miR-488, suppresses the expression of panic disorder gene pro-opiomelanocortin. [score:5]
Overexpression of miR-488 dysregulated corticotropin releasing hormone signalling, which is a crucial pathway activated in response to stress [25]. [score:4]
Muiños-Gimeno M. Espinosa-Parrilla Y. Guidi M. Kagerbauer B. Sipilä T. Maron E. Pettai K. Kananen L. Navinés R. Martín-Santos R. Human microRNAs miR-22, miR-138-2, miR-148a, and miR-488 are associated with panic disorder and regulate several anxiety candidate genes and related pathwaysBiol. [score:2]
miR-125b-2* and miR-488 peaked at 6 h from the onset of stroke, to 1.56 ± 0.28 and 1.36 ± 0.24 fold, respectively in ischemic rat brain whereas miR-27a*, -422a and -627 peaked at 24 h from the onset of stroke, to 5.37 ± 0.46, 1.52 ± 0.28 and 8.53 ± 1.23 fold, respectively (Figure 4). [score:1]
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[+] score: 11
The predicted expression profile of mir-488, which indicates that mir-488 mainly show high expression values in central nervous system. [score:5]
As shown in the Figure 2, each bar represents one tissue; the height of the bar represents the expression level of has-mir-488 in that tissue. [score:3]
For example, we predicted that hsa-mir-488 is high expressed in the amygdala, temporal lobe, globu spallidus, cerebellum peduncles, cerebellum, caudate nucleus, whole brain, parietal lobe, medulla oblongata, prefrontal cortex, occipital lobe, hypothalamus, thalamus, subthalamic nucleus, cingulated cortex, pons, spinal cord, fetal brain, adrenal gland, adrenal cortex and pituitary, which mainly belong to nervous systems except the adrenal gland and adrenal cortex (Figure 2). [score:3]
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[+] score: 10
Based on the collected miRNA-circRNA interactions and the deregulated RNA molecules, we collected several abnormally expressed miRNAs, including 11 downregulated miRNAs (miR-124-3p, miR-129-5p, miR-135a-5p, miR-153-3p, miR-204-5p, miR-208a-3p, miR-211-5p, miR-218-5p, miR-488-3p, miR-490-3p, and miR-504-5p) and 1 upregulated miRNA (miR-373-3p). [score:10]
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[+] score: 8
Subsequent RT-qPCR validated upregulated expression of miR-182, miR-488, miR-292, and miR-296, while miR-200a was downregulated in the mo del group compared to controls [32]. [score:8]
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[+] score: 5
For example, at least 8 miR, expressed in response to IFN-α, display RNA sequence specificity with the HCV genome, and of these, miR-351, miR-431 and miR-488 can functionally inhibit HCV replication [121]. [score:5]
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12
[+] score: 4
Other miRNAs from this paper: hsa-mir-622, mmu-mir-488
We also noticed that several potential PtpA -targeted ncRNA genes (such as miR-488, CASC2, and miR-622) are involved in tumor progression through regulating cell apoptosis, proliferation, and migration 55– 57. [score:4]
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[+] score: 4
Other miRNAs from this paper: hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3
There have been reports of other miRNAs regulating the expression of AR, including miR-488 [30]. [score:4]
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[+] score: 4
In fact, although some cellular miRNAs (e. g., hsa-miR-181c, hsa-miR-196, hsa-miR-199a, hsa-miR-488, and hsa-miR-let-7b) interact directly with viral genome inhibiting HCV replication (Piedade and Azevedo-Pereira, 2016b), one liver-specific miRNA, hsa-miR-122, binds to 5′ UTR region of HCV RNA enhancing viral genome replication and accumulation in infected cells (Jopling et al., 2005). [score:4]
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[+] score: 3
Target sites of two miRNA families, miR-488 and miR-329, are also very well conserved across both species. [score:3]
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[+] score: 3
Recently, Li et al. [22] showed that microRNA-488-3p sensitizes malignant melanoma cells to cisplatin by targeting PRKDC gene. [score:3]
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[+] score: 3
Examples of such miRNAs include those that show enriched expression in brain tissue such as miR-451 and miR-488 (see [32]) and miRNAs that have been implicated in the etiology of other tumor types, such as miR-346 in follicular thyroid carcinoma [36]. [score:3]
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[+] score: 3
10 miRNAs were consistently validated (Fig.   6) to be differentially expressed by HP diet, namely miR-592, miR-488-3p, miR-339-3p, miR-17-5p-1, miR-877-5p, miR-15b-5p, miR-484-1, miR-4745-5p, let-7b-5p and miR-25-3p. [score:3]
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[+] score: 3
They suggested miR-22 and miR-125 as possible master regulators, and miR-344-5p/484 and miR-488 as possible master coregulators that may influence the genes involved in one-carbon metabolism. [score:3]
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[+] score: 3
Genomic mapping of HTR2C transcripts (NM_000868, NM_001256760 and NM_001256761) and their six intragenic miRNAs (miR-1912, miR-764, miR-1264, miR-1298, miR-1911 and miR-488) as well as the expression correlation between HTR2C and these miRNAs. [score:3]
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[+] score: 2
On the other hand, miRNAs such as miR-22, miR-24, miR-29b, miR-34a, miR-125, miR-344-5p/484, and miR-488 were found to be strongly associated with the genes involved in the metabolic regulation of FOCM pathway [116, 117, 118]. [score:2]
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[+] score: 1
Other miRNAs from this paper: mmu-mir-488
We found that rs17737058, located in the 3′UTR of NCOA1 gene, causes the disruption of the binding with the hsa-miR-488* miRNA. [score:1]
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[+] score: 1
Other miRNAs from this paper: hsa-mir-548n
MicroRNA-488 regulates zinc transporter SLC39A8/ZIP8 during pathogenesis of osteoarthritis. [score:1]
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24
[+] score: 1
An asterisk is associated with the name of the miRNA that is not incorporated into the RISC complex (e. g., miR-488*). [score:1]
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25
[+] score: 1
Based on web databases analyses, six putative micro RNAs (miRNAs), hsa-miR-125b-2, hsa-miR-488, hsa-miR-657, hsa-miR-892a, hsa-miR-511, and hsa-miR-626, with one or more binding sites to the 3′UTR region of hCYP1A1 were identified [21]. [score:1]
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[+] score: 1
circ-NT5C2, 5′-AGTCCTAAGTTTTCCACTTCA-3′ (forward), 5′-AG GTGCCAGTAGCATTTTAGAC-3′ (reverse); miR-488, 5′-GCTGAGGGAGATATCGGCGCC-3′ (forward), 5′-GG AACACGCATGGCAGATCC-3′ (reverse); GAPDH, 5´-GCACCGTCAAGGCTGAGAAC-3´ (forward), 5´-TG GTGAAGACGCCAGTGGA-3′ (reverse). [score:1]
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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-21, hsa-mir-23a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-196a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-196a-2, hsa-mir-210, hsa-mir-181a-1, hsa-mir-218-1, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-30b, hsa-mir-128-1, hsa-mir-145, hsa-mir-191, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-30c-1, hsa-mir-99b, hsa-mir-296, hsa-mir-30e, hsa-mir-361, hsa-mir-337, hsa-mir-148b, hsa-mir-196b, hsa-mir-425, hsa-mir-20b, hsa-mir-486-1, hsa-mir-181d, hsa-mir-498, hsa-mir-519c, hsa-mir-520a, hsa-mir-526b, hsa-mir-520d, hsa-mir-506, hsa-mir-92b, hsa-mir-608, hsa-mir-617, hsa-mir-625, hsa-mir-641, hsa-mir-1264, hsa-mir-1271, bta-let-7f-2, bta-mir-103-1, bta-mir-148a, bta-mir-21, bta-mir-30d, bta-mir-128-1, bta-mir-145, bta-mir-181a-2, bta-mir-30b, bta-mir-181b-2, bta-mir-20b, bta-mir-30e, bta-mir-92a-2, bta-let-7d, bta-mir-148b, bta-mir-181c, bta-mir-191, bta-mir-210, bta-mir-23a, bta-mir-361, bta-mir-425, bta-let-7g, bta-mir-30a, bta-let-7a-1, bta-let-7f-1, bta-mir-30c, bta-let-7i, bta-mir-23b, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-103-2, bta-mir-99b, hsa-mir-890, hsa-mir-888, hsa-mir-889, hsa-mir-938, hsa-mir-1184-1, hsa-mir-1203, hsa-mir-1204, hsa-mir-1265, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-128-2, bta-mir-181d, bta-mir-196a-2, bta-mir-196a-1, bta-mir-196b, bta-mir-218-1, bta-mir-296, bta-mir-30f, bta-mir-486, bta-mir-488, bta-mir-92a-1, bta-mir-92b, bta-mir-1271, bta-mir-181a-1, bta-mir-181b-1, bta-mir-148c, hsa-mir-1184-2, hsa-mir-1184-3, hsa-mir-486-2, bta-mir-1264, bta-mir-148d
Among these, miR-938, miR-519c-3p, miR-1265, miR-498 and miR-488 were exclusively detected only in HE animals and 10 miRNAs including miR-608, miR-625*, miR-218-1*, miR-888*, miR-1184 and miR-1264 were detected only in SE and CE animal groups. [score:1]
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[+] score: 1
The secondary structure analysis of this chromosomal site including both precursors revealed another hairpin structure, which was not covered by miRDeep and possessed the conserved seed of miR-488 (data not shown). [score:1]
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