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10 publications mentioning gga-mir-107

Open access articles that are associated with the species Gallus gallus and mention the gene name mir-107. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 86
showed that miR-107 was able to decrease the expression of E2F1, while the miR-107 inhibitor could block the event in the cells (Figure 5C), suggesting that miR-107 inhibits the expression of E2F1 by targeting the 3′UTR of E2F1 mRNA. [score:11]
We found that miR-107 was able to decrease the expression of SPHK1 (supporting Figure 4B), suggesting that miR-107 decreases the expression of SPHK1 by targeting E2F1 mRNA 3′UTR. [score:7]
In addition, we observed that the overexpression of HULC resulted in the down-regulation of miR-107 in hepatoma cells (supporting Figure 4C), suggesting that the interaction of HULC with miR-107 results in the decrease of miR-107. [score:6]
showed that the overexpression of miR-107 suppressed the luciferase activities of pGL3-E2F1 in HepG2 cells (Figure 5A), but failed to work for pGL3-E2F1-mut in HepG2 and H7402 cells (Figure 5B). [score:5]
As expected, we revealed that miR-107 was able to bind the 3′UTR of E2F1 mRNA in hepatoma cells, resulting in the down-regulation of E2F1. [score:4]
HULC sequesters miR-107, resulting in the up-regulation of E2F1. [score:4]
HULC is able to up-regulate E2F1 by sequestering miR-107. [score:4]
It suggests that the interaction between HULC and miR-107 is responsible for the up-regulation of E2F1. [score:4]
Meanwhile, we validated that the overexpression of miR-107 also resulted in the decrease of HULC in hepatoma cells (supporting Figure 4D). [score:3]
To analyze miRNA-107 expression, total RNA was polyadenylated by poly (A) polymerase (Ambion, Austin, TX, USA) as described previously [39]. [score:3]
Accordingly, we supposed that HULC might inhibit miR-107, displaying a role of sponge. [score:3]
Given that HULC was capable of sequestering the miRNA to influence the gene expression [9], we observed that HULC potentially interacted with miR-107 through complementary base-pairs by bioinformatics analysis (http://bibiserv. [score:3]
MiR-107 mimics and its inhibitor (anti-miR-107) and their respective negative controls were from Ribobio Co. [score:3]
In addition, the expression levels of SPHK1 were determined by in HepG2 cells transfected with miR-107. [score:3]
Furthermore, we validated that the expression levels of HULC were negatively correlated with those of miR-107 in above 60 HCC tissues (P < 0. 001, r = −0.604, Pearson's correlation) (Figure 5F). [score:3]
Pearson's correlation coefficient was used to determine the correlation between the levels of SPHK1 (or S1P, or E2F1, or miR-107) and HULC mRNA in HCC tissues. [score:1]
B. Relative luciferase activities of pGL3-E2F1-mut were detected in HepG2 and H7402 cells treated with miR-107. [score:1]
Therefore, we selected miR-107 for further study. [score:1]
showed that HULC could abolish the decrease of pGL3-E2F1 luciferase activities mediated by miR-107 in HepG2 cells, but HULC-107-mut failed to work (Figure 5E), suggesting that the interaction between HULC and miR-107 is associated with the event. [score:1]
U6 was used as an internal control to normalize miRNA-107 levels. [score:1]
F. The correlation between HULC mRNA levels and miR-107 levels was detected by qRT-PCR in 60 HCC tissues (P < 0.001, r = −0.604, Pearson's correlation). [score:1]
Thereby, we concerned whether HULC blocked miR-107. [score:1]
We constructed the mutant of HULC (named HULC-107-mut) to confirm the interaction between HULC and miR-107 (Figure 5D). [score:1]
Our data showed that HULC could abolish the decrease of pGL3-E2F1 luciferase activities mediated by miR-107 in HepG2 cells, but HULC-107-mut failed to work. [score:1]
Interestingly, bioinformatics analysis showed that HULC was able to interact with miR-107 (Figure 5D), potentially displaying a sponge role. [score:1]
Bioinformatics analysis showed that miR-107 potentially bound 3′UTR of E2F1 mRNA. [score:1]
Then, we constructed the mutant of HULC, replacing the binding site of miR-107, to confirm the interaction between HULC and miR-107. [score:1]
We found that three miRNAs might bind the 3′UTR of E2F1 mRNA, including miR-107, miR-135 and miR-208b. [score:1]
D. A mo del shows the predicted interaction between HULC and miR-107 through complementary base-pairs. [score:1]
Our data showed that the tube formation was remarkably increased when the HUVECs were cultured with 50% (v/v) conditioned medium from HULC -transfected (or SPHK1 -transfected) HepG2 cells for 6 h (Figure 6 top), but the treatment with si-SPHK1-1 (or miR-107 or si-E2F1-1) obviously abrogated the HULC-enhanced tube formation in the system (Figure 6 bottom), suggesting that HULC contributes to the angiogenesis through HULC/miR-107/E2F1/SPHK1 signaling. [score:1]
Interestingly, our data show that HULC is capable of promoting tumor angiogenesis through miR-107/E2F1/SPHK1 signaling in hepatoma cells. [score:1]
HULC increases E2F1 by sequestering miR-107. [score:1]
Then we cloned the 3′UTR of E2F1 mRNA containing miR-107 binding site (termed pGL3-E2F1) and its mutant (termed pGL3-E2F1-mut) (supporting Figure 4A). [score:1]
In summary, in this study we report that HULC is able to promote the tumor angiogenesis through miR-107/E2F1/SPHK1 signaling in liver cancer. [score:1]
C. E2F1 was measured by in HepG2 and H7402 cells transfected with miR-107 or co -transfected with miR-107 and miR-107 inhibitor. [score:1]
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2
[+] score: 37
a ADIPOR2 is targeted by miR-20b and let-7c, b INSIG1 is targeted by miR-182, miR-183, and miR-454, c MAPK4K4 is targeted by miR-29a, d FASN is targeted by miR-107, e FADS2 is targeted by let-7c, f ELOVL2 is targeted by miR-10b, g HMGCS1 is targeted by miR-18a, and h MSMO1 is targeted by miR-20b and miR-454 To further explore miRNA regulatory networks associated with the metabolic switch, we identified potential metabolic mRNA targets for let-7c, miR-20b, and miR-183 using in silico target prediction in combination with IPA pathway analysis. [score:22]
Many SREBF1 regulated genes are also regulated by miRNAs, including let-7c, miR-200b, miR-107, and miR-18a Fig. 2Differential hepatic expression of a lipid metabolism network involving FADS2 and SCD and associated miRNA between E18 and D3 chickens. [score:5]
We found miR-107 to be downregulated in the posthatch liver. [score:4]
FASN mRNA is a miR-107 target (Figs.   2 and 3d). [score:3]
Many SREBF1-regulated genes are also regulated by miRNAs, including let-7c, miR-200b, miR-107, and miR-18a. [score:3]
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3
[+] score: 10
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-15a, hsa-mir-18a, hsa-mir-33a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-mir-27b, mmu-mir-126a, mmu-mir-128-1, mmu-mir-140, mmu-mir-146a, mmu-mir-152, mmu-mir-155, mmu-mir-191, hsa-mir-10a, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, mmu-mir-297a-1, mmu-mir-297a-2, hsa-mir-27b, hsa-mir-128-1, hsa-mir-140, hsa-mir-152, hsa-mir-191, hsa-mir-126, hsa-mir-146a, mmu-let-7a-1, mmu-let-7a-2, mmu-mir-15a, mmu-mir-18a, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-342, hsa-mir-155, mmu-mir-107, mmu-mir-10a, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-33, mmu-mir-211, hsa-mir-374a, hsa-mir-342, gga-mir-33-1, gga-let-7a-3, gga-mir-155, gga-mir-18a, gga-mir-15a, gga-mir-218-1, gga-mir-103-2, gga-mir-128-1, gga-mir-140, gga-let-7a-1, gga-mir-146a, gga-mir-103-1, gga-mir-218-2, gga-mir-126, gga-let-7a-2, gga-mir-27b, mmu-mir-466a, mmu-mir-467a-1, hsa-mir-499a, hsa-mir-545, hsa-mir-593, hsa-mir-600, hsa-mir-33b, gga-mir-499, gga-mir-211, gga-mir-466, mmu-mir-675, mmu-mir-677, mmu-mir-467b, mmu-mir-297b, mmu-mir-499, mmu-mir-717, hsa-mir-675, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-297c, 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-467c, mmu-mir-467d, mmu-mir-466d, hsa-mir-297, mmu-mir-467e, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-467f, mmu-mir-466j, mmu-mir-467g, mmu-mir-467h, hsa-mir-664a, hsa-mir-1306, hsa-mir-1307, gga-mir-1306, hsa-mir-103b-1, hsa-mir-103b-2, gga-mir-10a, mmu-mir-1306, mmu-mir-3064, mmu-mir-466m, mmu-mir-466o, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-466c-2, mmu-mir-467a-4, mmu-mir-466b-4, mmu-mir-467a-5, mmu-mir-466b-5, mmu-mir-467a-6, mmu-mir-466b-6, mmu-mir-467a-7, mmu-mir-466b-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, hsa-mir-466, hsa-mir-3173, hsa-mir-3618, hsa-mir-3064, hsa-mir-499b, mmu-mir-466q, hsa-mir-664b, gga-mir-3064, mmu-mir-126b, gga-mir-33-2, mmu-mir-3618, mmu-mir-466c-3, gga-mir-191
We also found opposing results regarding the expression of two miRNA/host gene pairs, murine mmu-mir-103/Pank3 and mmu-mir-107/Pank1– these have previously been demonstrated to have coordinate [71] as well as anti-correlative (or discordant) expression patterns [72]. [score:5]
Out of the 26 miRNA/host gene pairs with coordinated expression, 11 have been found to be coordinately expressed in both, human and mouse [19], [27], [59], [61]– [64], [67]– [69], [71], [73]– [79]: mir-103/ PANK3, mir-107/ PANK1, mir-126/ EGFL7, mir-128-1/ R3HDM1, mir-140/ WWP2, mir-211/ TRPM1, mir-218-1/ SLIT2, mir-218-2/ SLIT3, mir-27b/ C9orf3, mir-33/ SREBF2, and mir-499/ MYH7B. [score:5]
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4
[+] score: 7
In regions of AD brains with confirmed reduction of miR-107 expression, a significant increase in NFTs was observed when compared with adjacent tissue expressing normal levels of miR-107 [59]. [score:4]
Expression of the microRNA miR-107 has been shown to decrease in AD brain [60], which is associated with increased amyloid precursor protein and cofilin protein levels and formation of cofilin rod-like structures [61]. [score:3]
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5
[+] score: 6
miR-107, as a paralog of miR-103, was identified in human nonsmall cell lung cancer, and the potential target CCNE1 was downregulated by transfection with miR-107 (Takahashi et al. 2009). [score:6]
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6
[+] score: 6
HIF-1 was identified as target gene of miR-107 both in vitro and in vivo, suggesting a p53-miR-107-HIF-1 hypoxia response pathway [60]. [score:3]
miR-107 is directly regulated by p53, which is one of the most frequently mutated genes in human cancers [58]– [60]. [score:3]
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7
[+] score: 5
MicroRNA-107 functions as a candidate tumor-suppressor gene in head and neck squamous cell carcinoma by downregulation of protein kinase Cvarepsilon. [score:5]
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8
[+] score: 5
Similarly, some other highly expressed differential miRNAs (FDR < 0.05), such as miR-107-3p, let-7b, and miR-181b, have all been proved to take part in the regulation of postnatal liver development or metergasis process 22, 24, 25. [score:5]
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9
[+] score: 3
MiR-107 for example, inhibits dicer protein in zebrafish hindbrain, which normally activates miR-9 biogenesis and thus differentiation [65]. [score:3]
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10
[+] score: 3
For example, the three members of the let-7 family (let-7a, let-7f, let-7k) are broadly expressed across tissues [36] and tissue enrichment has been found for miR-499-5p and −3p in heart [37], miR-122-5p in liver [38], miR-202-5p in testis [39] and gga-miR-107-3p in brain tissues [40] (Table 2). [score:3]
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