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8 publications mentioning gga-mir-103-2

Open access articles that are associated with the species Gallus gallus and mention the gene name mir-103-2. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 216
The RNA expression of gga-miR-103-3p, CCNE1, and TFDP2 in MDCC-MSB1 cells was examined at 24 hr, 48 hr, and 72 hr after transfecting gga-miR-103-3p mimics, mimics NC, gga-miR-103-3p inhibitor, and inhibitor NC, respectively. [score:7]
Figure 4Protein expression levels of CCNE1, TFDP2, and ACTIN at 72 hr in MDCC-MSB1 cells after transfecting gga-miR-103-3p mimics, mimics NC, gga-miR-103-3p inhibitor, and inhibitor NC, respectively. [score:7]
of target mRNA expression and western blot assay indicated that gga-miR-103-3p regulated CCNE1 gene expression at both mRNA and protein levels. [score:7]
The protein expression levels of CCNE1 and TFDP2 were detected in MDCC-MSB1 cells at 72 hr after transfection with gga-miR-103-3p mimics, mimics NC, gga-miR-103-3p inhibitor, and inhibitor NC, respectively. [score:7]
The expression of CCNE1 at 72 hr after transfecting MDCC-MSB1 cells with gga-miR-103-3p inhibitor was notably increased compared with the inhibitor NC group, which indirectly indicated that gga-miR-103-3p could bind with CCNE1 (Figure 3B). [score:7]
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]
As shown in Figure 5B, the migrated cell number in the gga-miR-103-3p mimics transfection group was notably decreased compared with the mimics NC group, suggesting that overexpression of gga-miR-103-3p could inhibit MDCC-MSB1 cell migration at 48 h. Collectively, gga-miR-103-3p could suppress MDCC-MSB1 cell migration, but has no obvious effects on its proliferation. [score:6]
Gga-miR-103-3p could suppress CCNE1 gene expression at both mRNA and protein levels, while the TPDP2 gene was regulated by gga-miR-103-3p at the protein but not mRNA level. [score:6]
In summary, we found that gga-miR-103-3p was downregulated in MDV-infected tissues, and it inhibits cell migration in MDCC-MSB1 cell lines. [score:6]
The results demonstrated that gga-miR-103-3p could interfere with expression of CCNE1 mRNA, but did not regulate TFDP2 mRNA expression. [score:6]
The results showed that expression of gga-miR-103-3p was significantly downregulated in tumorous spleen and MD lymphoma from liver compared with the noninfected tissues (Figure 1). [score:5]
A total of 1 × 10 [4] MDCC-MSB1 cells per well were seeded into 96-well plates, and transfected with gga-miR-103-3p mimics, mimics NC, gga-miR-103-3p inhibitor, and inhibitor NC, respectively. [score:5]
MDCC-MSB1 cells were seeded into six-well plates, and transfected with gga-miR-103-3p mimics, mimics NC, gga-miR-103-3p inhibitor, and inhibitor NC, respectively. [score:5]
As shown in Figure 3, the expression level of gga-miR-103-3p was significantly higher in the gga-miR-103-3p mimics group, and lower in the gga-miR-103-3p inhibitor transfection group than that in corresponding negative control, respectively (Figure 3A). [score:5]
Sequences of gga-miR-103-3p mimics, mimics negative control (NC), inhibitor, and inhibitor NC (GenePharma, Shanghai, China). [score:5]
The gga-miR-103-3p mimics, mimics NC, gga-miR-103-3p inhibitor, and inhibitor NC were transfected into MDCC-MSB1 cells with FuGENE HD transfection reagent, respectively. [score:5]
File S1 contains the target genes of gga-miR-103-3p predicted by TargetScan and miRDB, and clustered by GO analysis. [score:5]
The results showed that the protein levels of CCNE1 and TFDP2 were significantly reduced after transfection with gga-miR-103-3p mimics compared with mimics NC, and the relative protein expression of these two genes in gga-miR-103-3p inhibitor groups were notably increased compared to inhibitor NC groups, respectively (Figure 4). [score:5]
The target genes of gga-miR-103-3p were predicted using the online tools TargetScan (http://www. [score:5]
In MDV-infected chickens of line 7 [2] (MD susceptible line), the expression of gga-miR-103 was significantly downregulated compared with noninfected chickens at 21 dpi (Tian et al. 2012). [score:5]
From the point of view of cancer or tumor research, it was reported that miR-103 is part of the G1/S transition regulatory network, by targeting CCNE1, CDK2, and CREB1 (cAMP responsive element binding protein 1) during IGF-1 simulated proliferation in mouse crypt cells (Liao and Lonnerdal 2010). [score:4]
The binding sites of gga-miR-103-3p in the 3ʹ-UTR of target genes were confirmed by luciferase reporter assay, and the expression of target genes in mRNA, and protein levels, were validated using real-time PCR and western blot analysis, respectively; moreover, the biological function of gga-miR-103-3p in cell proliferation and migration was investigated. [score:4]
The gga-miR-103-3p mimics group was compared with mimics NC group, and inhibitor NC group was the control for gga-miR-103-3p inhibitor group. [score:4]
In this study, we identified a binding site of gga-miR-103-3p in the 3′UTR of CCNE1, and verified that CCNE1 was a target gene of gga-miR-103-3p. [score:3]
The expression of gga-miR-103-3p, and the two targets, were measured using the 2 [–ΔΔCt] method. [score:3]
MiR-103/107 overexpression or CDK5R1 [cyclin -dependent kinase 5, regulatory subunit 1 (p35)] silencing caused a reduction in SK-N-BE migration ability (Moncini et al. 2011). [score:3]
Gga-miR-103-3p, working together with its targets, may play a potential role in MDV tumorigenesis. [score:3]
The expression of gga-miR-103-3p among tumorous spleen, MD lymphoma from liver, noninfected spleen, and noninfected liver, was detected by qPCR. [score:3]
Differential expression of gga-miR-103-3p between MDV-infected and noninfected groups. [score:3]
It was reported that miR-103 was differentially expressed in lung cancer (Garofalo et al. 2012), colorectal cancer (Chen et al. 2012), human gastric carcinoma (Zhang et al. 2015), and breast cancer (Kleivi Sahlberg et al. 2015). [score:3]
Prediction and verification of gga-miR-103-3p target genes. [score:3]
As for MD, it was reported that gga-miR-103-3p was expressed differentially between MDV-infected and uninfected CEF cells (Burnside et al. 2008). [score:3]
Figure 1Differential expression of gga-miR-103-3p among tumorous spleen, noninfected spleen, MD lymphoma from liver, and noninfected liver. [score:3]
Our results suggested that gga-miR-103-3p suppressed cell migration in the MDCC-MSB1 cell line. [score:3]
RNA isolation and real-time PCR for quantifying gga-miR-103-3p expression in tissue. [score:3]
Chicken 5S rRNA and GAPDH were the endogenous reference for gga-miR-103-3p and the two target genes, respectively. [score:3]
Figure 5Effects of gga-miR-103-3p on cell proliferation and migration of Marek’s disease lymphoma cell line (MDCC-MSB1) cells. [score:3]
Figure 3Expression of (A) gga-miR-103-3p, (B) CCNE1, and (C) TFDP2 at 24 hr, 48 hr, and 72 hr. [score:3]
Total RNA was isolated at 24 hr, 48 hr, and 72 hr after transfection, and real-time PCR was performed as described above for validating the expression of gga-miR-103-3p. [score:3]
Overall, CCNE1 and TFDP2 are the two candidate target genes for gga-miR-103-3p. [score:3]
These results suggest that gga-miR-103-3p could bind to three sites in the target TFDP2 mRNA. [score:3]
On the contrary, expression of CCNE1 was significantly lower at 48 hr after transfection with gga-miR-103-3p mimics compared with the mimics NC group. [score:2]
The results showed that relative luciferase activity of CCNE1 wt UTR reporter was significantly inhibited by 40% when cotransfected with gga-miR-103-3p mimics compared with mimics NC (Figure 2B). [score:2]
Real-time PCR primers for detecting expression of gga-miR-103-3p. [score:2]
Several studies have shown that miR-103 is involved in cancers, and in regulated cell proliferation and migration. [score:2]
To explore the role played by gga-miR-103-3p in MDCC-MSB1 cells, we performed cell proliferation and migration assays after overexpressing or interfering with gga-miR-103-3p. [score:2]
The proliferation and migration of CRC cells could be regulated by miR-103 (Hong et al. 2014). [score:2]
However, the cell viability exhibited no obvious change at 24 hr, 48 hr, and 72 hr in gga-miR-103-3p mimics or gga-miR-103-3p inhibitor groups, compared with the corresponding NC group (Figure 5A). [score:2]
The expression of gga-miR-103-3p was measured using the 2 [–ΔΔCt] method. [score:1]
Then, pmiR-RB-Report luciferase reported vector containing wild type or mutant type were cotransfected with gga-miR-103-3p mimics, or NC, into HEK 293T cells using FuGENE HD transfection reagent (Promega, Madison, WI). [score:1]
Taken together, the results demonstrate strongly that the CCNE1 (248–254) UTR was not the binding site of gga-miR-103-3p. [score:1]
In recent years, only a few studies on chicken gga-miR-103 have been reported, including deep sequencing in chicken preadipocytes (Yao et al. 2011), hypothalamus tissue (Sun et al. 2012), chromium metabolism (Pan et al. 2013), abdominal fatness (Wang et al. 2015), and abdominal adipose tissues (Huang et al. 2015). [score:1]
Our results showed that gga-miR-103-3p was greatly decreased in MDV-infected tissues, which is consistent with the previous studies (Burnside et al. 2008; Tian et al. 2012). [score:1]
cgi?mirg=gga-miR-103). [score:1]
The relative luciferase activities of TFDP2 wt (1–1252) UTR and TFDP2 wt (5161–6415) UTR reporters cotransfected with gga-miR-103-3p mimics were both significantly decreased (Figure 2D). [score:1]
Briefly, fragments of 3ʹ-UTR sequences covering the putative gga-miR-103-3p binding sites were amplified, and then inserted into pmiR-RB-REPORT luciferase reporter vectors to construct wild-type 3ʹ-UTR vector. [score:1]
The effective binding sites of gga-miR-103-3p in the 3ʹ-UTR of CCNE1 and TFDP2 mRNA were confirmed. [score:1]
A vital molecular relationship between miR-103 and PER3 (period circadian clock 3) in human colorectal cancer (CRC) cell lines was confirmed. [score:1]
The CCNE1 (75–81) UTR and CCNE1 (475–481) UTR could bind gga-miR-103-3p, and the CCNE1 (75–81) UTR was the primary binding site of gga-miR-103-3p. [score:1]
The three mutant-type reporters, including CCNE1 mut (75–81) UTR, CCNE1 mut (248–254) UTR, and CCNE1 mut (475–481) UTR reporter, were cotransfected with gga-miR-103-3p mimics, and mimics NC, respectively. [score:1]
These two reporters have one and two binding sites for gga-miR-103-3p, respectively. [score:1]
The effects of gga-miR-103-3p on cell proliferation and migration. [score:1]
However, gga-miR-103-3p could modulate TFDP2 at the protein but not the mRNA level. [score:1]
The gga-miR-103-3p mimics and mimics negative control (NC) were synthesized by GenePharma (Shanghai, China; Table 3). [score:1]
Although, miR-103 has been investigated extensively in mammalian diseases, studies on gga-miR-103 in chickens are still limited. [score:1]
CCNE1 mut (75–81) UTR and CCNE1 mut (475–481) UTR had no significant change, but the relative luciferase activities of CCNE1 (475–481) UTR displayed a downtrend when this reporter was cotransfected with gga-miR-103-3p mimics (Figure 2B). [score:1]
This suggested that gga-miR-103-3p could not influence MDCC-MSB1 cell proliferation. [score:1]
The miR-103 family has been found in 23 species (Griffiths-Jones 2004; Griffiths-Jones et al. 2006). [score:1]
Here, we verified that TFDP2 was another target gene of gga-miR-103-3p by luciferase reporter assay and western blot assay. [score:1]
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2
[+] score: 18
The DEM miR-103 was up-regulated, and it regulates glucose homeostasis and insulin sensitivity in obese mice 28 and up-regulates many marker genes and triglycerides in 3T3-L1 cells 29. [score:8]
Eleven of these (miR-204, miR-19a-3p, miR-19b-3p, miR-30d, miR-26a, miR-122-5p, miR-103-3p, miR-27b-3p, miR-92-3p, miR-142-3p, and miR-17-5p) have been implicated, directly or indirectly, in fat deposition; 9 showed a high fold-change (miR-3535, miR-144-3p, miR-30e-5p, miR-301b-3p, miR-215-5p, miR-200a-3p, miR-133a-3p, miR-133c-3p, and miR-146b-5p). [score:3]
Specifically, the integrated analysis of DEMs and DEGs suggests that nine miRNAs (gga-miR-19a-3p, miR-19b-3p, miR-17-5p, miR-30d, miR-26a, miR-103-3p, miR-27b-3p, miR-142-3p, and miR-92-3p) and three genes (ACSL1, FADS2 and ABCD3) are strong candidate miRNAs and genes involved in regulating the accumulation of AbF in chickens. [score:2]
With the exception of miR-204, miR-215-5p, miR-142-3p, and miR-103-3p, there was consistency between the qPCR assays and the deep sequencing analysis in terms of the direction of regulation and statistical significance (Fig. 1). [score:2]
Some of the DEMs identified by deep sequencing (miR-19a-3p, miR-19b-3p, miR-30d, miR-26a, miR-30a-5p, miR-122-5p, miR-103, miR-125b, and miR-17-5p) are known to influence mammalian lipid metabolism. [score:1]
Changes in four lipid-related DEMs identified by deep sequencing (gga-miR-122-5p, miR-103-3p, miR-27b-3p, and miR-146b-5p) were confirmed by qPCR. [score:1]
However, many important candidate miRNAs related to lipid mechanism (e. g., gga-miR-301b-3p, gga-miR-130b-3p, gga-miR-30a-5p, gga-miR-142, gga-miR-146b, gga-miR-103, gga -miR-26a, etc. ) [score:1]
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[+] score: 14
These miRNAs were divided into three groups according to their expression levels in the fat broiler line, 4 highly expressed (gga-miR-21, gga-miR-148a, gga-miR-103, gga-miR-101) (2 [-ΔCt] >0.7), 4 moderately expressed (gga-miR-100, gga-miR-146a, gga-miR-92, gga-miR-2188) (0.7>2 [-ΔCt]>0.08), and 7 lowly expressed (gga-miR-1a, gga-miR-130a, gga-miR-221, gga-miR-19a, gga-miR-181b, gga-miR-458, gga-miR-17–3p) (2 [-ΔCt]<0.08) (Table 2). [score:9]
In mammals, a number of miRNAs have been demonstrated to target genes involved in adipogenesis and lipid metabolism, such as the regulation on the proliferation of adipose tissue-derived mesenchymal stem cells by miR-21 and miR-196a [4– 6]; the enhancement of adipogenesis by miR-103, miR-224 and the miR-17–92 cluster [7– 9]; the impairment of adipogenesis by the let-7 family, miR-448, miR-15a and miR-27 [10– 13]; the regulation of adipocyte lipid metabolism by miR-27a and miR-143 [13– 15]; and the important role of miR-33 on the repression of sterol transporters reported in numerous studies [16– 24]. [score:5]
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[+] score: 10
For example, a comparison of miRNA expression profiles in proliferating myoblasts and differentiated myotubes revealed that miR-221 and miR-222 are down-regulated upon differentiation of primary and established myogenic cells, whereas miR-21, miR-103, miR-130, miR-99, miR-30 and miR20 are up-regulated [19, 33], suggesting that these miRNAs play important roles in the transition between proliferation and differentiation of muscle cells. [score:9]
In addition to miR-206, miR-1 and miR-181, nine other miRNAs among the most abundant in these libraries (miR-221, miR-222, miR-21, miR-103, miR-130, miR-99, miR-30, miR20, and miR128) have been implicated in the proliferation and differentiation of muscle cells (Table 1) [15, 19, 33]. [score:1]
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5
[+] 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-107, 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
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]
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]
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6
[+] score: 6
Except for gga-miR-92-5p with a slight difference in the R group, the expression patterns of gga-miR-101-3p, gga-miR-126-3p, gga-miR-155, gga-miR-103-5p, and gga-miR-455 were comparable by both methods. [score:3]
LRRC59 was predicted as a potential target of gga-miR-103-5p and gga-miR-155. [score:3]
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7
[+] score: 5
Top amongst them were miRs reported to decrease tumor metastasis and invasion (miR-194, miR-103, miR-29) [21, 22], inhibit cell proliferation (let-7 family, miR-215) [23], induce apoptosis (miR-125) [24], and tumor suppressors (let-7 family, miR-125, miR-106) [25, 26] to mention but a few. [score:5]
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8
[+] score: 2
Furthermore, in the E11_VS_E16 contrast group, 8 miRNAs (miR-203a, miR-6561-5p, miR-460a-5p, miR-205a, miR-3536, miR-103-3p miR-205b, and miR-200b-3p) were highly regulated. [score:2]
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