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23 publications mentioning gga-mir-221

Open access articles that are associated with the species Gallus gallus and mention the gene name mir-221. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 198
Given that gga-miR-221 and gga-miR-222 promote the proliferation, migration, and growth of DF-1 cells, and inhibit the apoptosis of DF-1 cells by suppressing the expression of BMF, we assessed the expression level of BMF mRNA in SPF chickens infected with ALV-J. In the liver, the level of BMF mRNA was downregulated 10 and 70 days after infection (Figure 5A). [score:12]
Despite the link to increased expression of miR-221 and miR-222 in MDV infection, there has not been a comprehensive study assessing gga-miR-221 and gga-miR-222 expression in chickens infected by ALV-J. To understand more fully whether there is a correlation between differential expression of gga-miR-221 and gga-miR-222 and ALV-J pathogenesis, we examined the functions of gga-miR-221 and gga-miR-222 in cell proliferation, migration, and apoptosis in vitro, and determined the expression levels of gga-miR-221 and gga-miR-222 in ALV-J infection in vivo. [score:9]
Galardi et al. [35], suggested that the regulatory factor of cell cycle p27 (Kip l) may be a target of miR-221 and miR-222 regulation, and found that the quantity of p27 in pancreas cells was negatively correlated with the expression level of miR-221 and miR-222, suggesting they likely regulate cell proliferation and the cell cycle. [score:8]
The level of BMF protein in cells over -expressing gga-miR-221 and gga-miR-222 were reduced compared to the NC and control groups (Figure 4D), suggesting that over-expressed gga-miR-221 and gga-miR-222 inhibit the expression of BMF. [score:8]
3.4. gga-miR-221 and gga-miR-222 Inhibit the Expression of BMF by Binding to the 3′-Untranslated Region (UTR). [score:7]
Lambeth et al. [38], have reported increased expression of Gallus gallus (gga)-miR-221 and gga-miR-222 in poultry in the cancer cell line MSB-1 transformed by MDV (Marek’s Disease Virus), suggesting a link between oncogenic poultry viruses and expression levels of miR-221 and miR-222. [score:7]
In this study, we provide evidence that gga-miR-221 and gga-miR-222 are up-regulated in the livers of pullets infected with ALV-J. Furthermore, we demonstrate that gga-miR-221 and gga-miR-222 have stimulating effects on cell growth and proliferation, and that BMF is a likely target for gga-miR-221 and gga-miR-222. [score:6]
We first examined the expression levels of gga-miR-221 and gga-miR-222 in vivo in pullets infected with ALV-J. Gene chip analysis indicated that miR-221 and miR-222 were up-regulated significantly in the livers of infected pullets 10 days post infection (Figure 1B). [score:6]
Taken together, our results and studies in the Marek’s disease virus (MDV) mo del suggest that up-regulation of gga-miR-221 and gga-miR-222 might be a general feature of oncogenic poultry viruses. [score:6]
Therefore, analyses to detect the expression of miRNAs and genes could possibly elucidate the tumorigenic mechanisms of ALV-J. Taken together, our results suggest that miR-221 and miR-222 regulate BMF and inhibit apoptosis through the mitochondrial pathway. [score:6]
Figure 1gga-miR-221 and gga-miR-222 expression was upregulated in ALV-J induced cancer. [score:6]
The amplified putative binding sites for miR221 and miR-222 in the 3′ UTR sequence were inserted downstream of the stop codon of firefly luciferase in the pmiR-GLO Dual-Luciferase miRNA Target Expression Vector (Ambion, Promega, Beijing, China). [score:5]
Over -expression of miR-221 is associated with a more aggressive phenotype of hepatocellular carcinoma and inhibits apoptosis by binding to BMF. [score:5]
Gramantieri et al. [37], demonstrated that BMF is a target of miR-221 and may play a role in mediating miR-221 -induced inhibition of apoptosis in hepatocellular carcinoma. [score:5]
The target genes of gga-miR-221 and gga-miR-222 were predicted utilizing online databases such as TargetScan, PicTar, and MicroCosm. [score:5]
Given the over -expression levels of miR-221 and miR-222 in terminal malignant tumors, they are likely therapeutic targets for carcinoma. [score:5]
Galardi S. Mercatelli N. Giorda E. Massalini S. Frajese G. V. Ciafrè S. A. Farace M. G. MiR-221 and miR-222 expression affects the proliferation potential of human prostate carcinoma cell lines by targeting p27Kip1 J. Biol. [score:5]
Inhibition of miR-221 and miR-222 could possibly inhibit growth and induce apoptosis in cells [36]. [score:5]
Figure 4BMF is a direct target for gga-miR-221 and gga-miR-222. [score:4]
In chickens, miR-221 and miR-222 are located on chromosome 1. Our previous study has shown that gga-miR-221 and gga-miR-222 to be frequently up-regulated in the livers of chickens 10 weeks post ALV-J infection [29]. [score:4]
Thus, by regulating miR-221 and miR-222, ALV-J, promotes the proliferation, migration, and growth of cells, and inhibits apoptosis to induce tumor formation. [score:4]
3.3. gga-miR-221 and gga-miR-222 Inhibit Apoptosis. [score:3]
The predicted results identified BMF as a target gene of gga-miR-221 and gga-miR-222 (Figure 4A). [score:3]
Zhang C. Zhang J. Zhang A. Wang Y. Han L. You Y. Pu P. Kang C. PUMA is a novel target of miR-221/222 in human epithelial cancers Int. [score:3]
QRT-PCR was used to confirm that the levels of gga-miR-221 were significantly up-regulated in the livers of the infected pullets compared to the control group at each time point examined, except for the 20-day-old time point (p < 0.01; Figure 1C). [score:3]
In poultry, Li et al. [27], have reported gga-miR-375 may function as a tumor suppressor in infection of ALV-J. MiR-221 and miR-222, are examples of miRNA that is highly conserved among chordates and is located on the X chromosome in humans, rats, and mice [28]. [score:3]
They also provided evidence that gga-miR-221 and gga-miR-222 inhibit p27 (Kip l). [score:3]
Expression of gga-miR-221 and gga-miR-222 in the Liver and Marrow of Pullets Infected with ALV-J. 3.2. gga-miR-221 and gga-miR-222 Accelerate the Proliferation, Growth, and Migration of DF-1 Cells. [score:3]
To understand the possible impacts of gga-miR-221 and gga-miR-222 on ALV-J tumorigenesis, we assessed the effects of over -expressing the miRNAs on the proliferation of DF-1 cells over three days. [score:3]
These results reaffirmed the anti-apoptotic effects of over -expressing gga-miR-221 and gga-miR-222. [score:3]
Gga-miR221 and gga-miR-222 expression was normalized to the 5s snRNA (chicken), and Bmf were normalized to HMBS (chicken). [score:3]
As it has been confirmed as the target gene of gga-miR-221/222 in our experiments. [score:3]
DA represents the control group and A represents tte infection group; (C) and (D) gga-miR-221 and gga-miR-222 expression levels in the liver of ALV-J infected chickens were quantified by qRT-PCR every 10 days from 10 to 70 days (** p < 0.01; * p < 0.05). [score:3]
The relative expression levels of gga-miR221, gga-miR-222, bmf by RT-qPCR. [score:3]
Figure 3gga-miR-221 and gga-miR-222 inhibit apoptosis induced by serum starvation, cisplatin, and doxorubicin. [score:3]
Miller T. E. Ghoshal K. Ramaswamy B. Roy S. Datta J. Shapiro C. L. Vlatkovic I. Kralovics R. Cerny-Reiterer S. Valent P. MicroRNA-221/222 confers tamoxifen resistance in breast cancer by targeting p27Kip1 J. Biol. [score:2]
The level of apoptosis level in DF-1 cells that were transfected with gga-miR-221 and gga-miR-222 was substantially reduced compared to the NC groups and the control group, suggesting that the over -expression of gga-miR-221 and gga-miR-222 has anti-apoptotic effects (Figure 3A,B). [score:2]
Gramantieri L. Fornari F. Ferracin M. Veronese A. Sabbioni S. Calin G. A. Grazi G. L. Croce C. M. Bolondi L. Negrini M. MicroRNA-221 targets Bmf in hepatocellular carcinoma and correlates with tumor multifocality Clin. [score:2]
Gga-miR-221, gga-miR-222, and normal control (NC) mimics transfected into DF-1 cells in triplicate in 24-well plates at 1.6 × 10 [5] cells/well. [score:1]
DF-1 cells were co -transfected with gga-miR-221, gga-miR-222, miR-NC and either wt-BMF-3′ UTR (left) or mut-BMF-3′ UTR (right). [score:1]
These results provided additional support that gga-miR-221 and gga-miR-222 effect the growth and migration of DF-1 cells. [score:1]
To better understand the anti-apoptotic function of gga-miR-221 and gga-miR-222, apoptosis was induced using three different methods, serum starvation, cisplatin treatment, and doxorubicin treatment. [score:1]
Magnification is 200× (B) The differences in the rate of apoptosis between gga-miR-221, gga-miR-222, miR-NC, and mock transfected cells are shown. [score:1]
MiRNA mimics for gga-miR-221, gga-miR-222, and the NC mimics were transfected into DF-1 cells in triplicate at 40 nM. [score:1]
Serum starved DF-1 cells that were transfected with gga-miR-221 and gga-miR-222 displayed relatively low rates of apoptosis, confirming that gga-miR-221 and gga-miR-222 are anti-apoptotic when cells are malnourished. [score:1]
Cells were transfected with gga-miR-221, gga-miR-222, miR-NC, or mock transfected and then stained with DAPI. [score:1]
DF-1 cells were transfected with gga-miR-221 and gga-miR-222 for 72 h and then the proteins were harvested for Western blot. [score:1]
The cells reached 80%–90% confluence after 24 h. The DF-1 cells were transfected 10 nmol/L gga-miR-221 and gga-miR-222 mimics 20 ng BMF-3’UTR-wt, or BMF-3’UTR-mut, and 4 ng pRL-TK (Promega). [score:1]
The gga-miR-221 is identical to Homo sapiens (hsa)-miR-221 and Mus musculus (muu)-miR-221 while the gga-miR-222 differs from hsa-miR-222 and muu-miR-222 by three bases (Figure 4B). [score:1]
DF-1 cells were transfected with gga-miR-221, gga-miR-222, NC miRNA, or mock transfected and then induced to undergo apoptosis using serum starvation (48 h), cisplatin treatment (72 h), or doxorubicin treatment (72 h). [score:1]
Similarly, cells transfected with gga-miR-221 and gga-miR-222 were resistant to doxorubicin -induced apoptosis. [score:1]
In our study, cells transfected with gga-miR-221 and gga-miR-222 were relatively resistant to cisplatin -induced apoptosis. [score:1]
Gga-miR-221, gga-miR-222, and NC mimics were transfected into DF-1 cells in triplicate in 24-well plates at 1.6 × 10 [5] cells/well. [score:1]
DF-1 cells were transfected with miRNA mimics for gga-miR-221, gga-miR-222 (Shanghai GenePharma Co. [score:1]
The percentage of cells undergoing apoptosis after transfection with gga-miR-221 was: 21% after serum starvation, 31.1% after cisplatin treatment, and 13.7% after doxorubicin treatment. [score:1]
DF-1 cells were transfected with the gga-miR-221, gga-miR-222, and NC mimics in six-well plates at 2 × 10 [5] cells/well. [score:1]
Twenty-four hours after plating, gga-miR-221, gga-miR-222, and negative control mimics were transfected into the DF-1 cells in triplicate. [score:1]
The relative expression levels of gga-miR-221, gga-miR-222, and Bmf were calculated using the 2 [−△△] [C] [T] method. [score:1]
Figure 2gga-miR-221 and gga-miR-222 promoted DF-1 cell proliferation and invasion. [score:1]
We have deposited the sequences of gga-miR-221 and gga-miR-222 (MI0001178, MI0001177) described in this paper in miRBase. [score:1]
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[+] score: 70
In the current study, expression of miR-221 and miR-222 was down-regulated in MDV-infected samples, especially in MD lymphoma, which was consistent with a previous report that miR-221 was slightly down-regulated in MDV -induced splenic tumors [18]. [score:9]
Of these 39 miRNAs, four down-regulated miRNAs (gga-miR-221, −140*, −199*, and 181a) and four up-regulated miRNAs (gga-miR-146c, −146b, −222, and −155) in the two MDV-infected samples with high counts were selected to be further verified by qPCR among MDV-infected whole spleens with tumors (tumorous spleens), MD lymphomas from liver, and non-infected spleens. [score:7]
However, the increased expression was unique to the MSB1 cell line, while in some other MDV transformed cell lines, such as MDCC-226S (T226S) and MDCC-265L (T265L), levels of miR-221 and miR-222 were unchanged or down-regulated [61]. [score:6]
Six miRNAs (gga-miR-181a, gga-miR-26a, gga-miR-221, gga-miR-222, gga-miR-199*, and gga-miR-140*) were down-regulated and one miRNA (miR-146c) was up-regulated in MDV-infected samples, and especially in MD lymphomas, compared to non-infected samples. [score:6]
Although BCL11B is likely not the target gene of miR-221, its involvement in tumorigenesis is still suggested because of its up-regulation in MD tumors. [score:6]
Putative target genes of gga-miR-181a, gga-miR-26a, gga-miR-221, gga-miR-222, gga-miR-155, gga-miR-146b, and gga-miR-146c were predicted by TargetScan (Version 6.0) [31]. [score:5]
gga-miR-181a, gga-miR-26a, gga-miR-221, gga-miR-199*, and gga-miR-140* were down-regulated (Figure 2A–E). [score:4]
Up-regulation of miR-221 and miR-222 was observed in MSB1 [22], [23], [61]. [score:4]
BCL11B, as a predicted target for miR-221 and miR-199*, has been implicated in T-cell development, differentiation, and proliferation [69]. [score:4]
The differential expression profiles of seven miRNAs (gga-miR-221, −140*,−199*, 181a, −146b, −146c, and −26a) were consistent between IDEG6 analysis and qPCR. [score:3]
C. Expression of gga-miR-221 among TS, LL, and NS. [score:3]
Both miR-221 and miR-222 were over-expressed in tumors of the lung, breast, pancreas and in glioblastoma, and papillary thyroid carcinoma, [37], [63]– [66]. [score:3]
To further verify the interaction of predicted target genes and miRNAs, we conducted luciferase reporter gene assays to detect interaction of gga-miR-181a with MYBL1 and IGF2BP3, gga-miR-26a with EIF3A, and gga-miR-221 with BCL11B. [score:2]
The regulation of miR-221 in different cancer types appears to be variable. [score:2]
Some predicted target genes for miR-221, 222, and 199*, such as RUNX2, BCL11B, and RAB1A, show oncogenic characteristics in tumors. [score:1]
A. Schema of binding site for gga-miR-181a and MYBL1; B. Schema of binding site for gga-miR-181a and IGF2BP3; C. Schema of binding site for gga-miR-26a and EIF3A; D. Schema of binding site for gga-miR-221 and BCL11B. [score:1]
The gga-miR-181a mimic, gga-miR-26a mimic, gga-miR-221 mimic and their corresponding negative controls (Ribobio Co. ) [score:1]
D. Interaction validation for gga-miR-221 and BCL11B. [score:1]
The gga-miR-221 mimic slightly decreased luciferase activity of pmiR-RB-REPORT-BCL11B UTR by 12% (Figure 5D). [score:1]
0051003.g004 Figure 4 A. Schema of binding site for gga-miR-181a and MYBL1; B. Schema of binding site for gga-miR-181a and IGF2BP3; C. Schema of binding site for gga-miR-26a and EIF3A; D. Schema of binding site for gga-miR-221 and BCL11B. [score:1]
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[+] score: 22
Other miRNAs from this paper: gga-mir-155
miR-221 targets the cyclin -dependent kinase inhibitor 1B (p27, Kip1), a regulator of the cell cycle G1 to S phase transition. [score:6]
Although HVT is non-oncogenic, expression of a miR-221 ortholog and down-regulation of p27 could move the cell cycle to the S phase in order to support replication of the viral genome as well as to increase growth of infected cells for additional viral production. [score:6]
MDV1 and HVT encode homologs of the host microRNA, miR-221, which targets a gene important in cell cycle regulation. [score:4]
In the chicken, miR-221 is very abundant in CEFs and other tissues [12, 20, 21], and it is likely that expression is similar in the turkey, which is the natural host of HVT. [score:3]
The repression of p27 by miR-221 is thought to play an important role in cancer progression [22, 23], and could play a role in MDV1 -induced tumorigenesis {Lambeth, 2009 #5006}. [score:1]
MDV1 contains a microRNA (mdv1-miR-M32) that shares a seed sequence with miR-221 {Morgan, 2008 #4818}. [score:1]
One of the HVT microRNAs, hvt-miR-H14-3p, is a homologue of gga-miR-221 with 21/23 nucleotide identity, including complete conservation of the seed/family sequence. [score:1]
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[+] score: 21
The expression of a miR-221 ortholog and down-regulation of p27 could move the cell cycle to the S phase in order to support replication of the viral genome as well as to increase growth of infected cells for additional viral production [38]. [score:6]
Interestingly, miR-221 targets the cyclin -dependent kinase inhibitor 1B (p27, Kip1), a regulator of the cell cycle G1 to S phase transition. [score:6]
Galardi S. Mercatelli N. Giorda E. Massalini S. Frajese G. V. Ciafre S. A. Farace M. G. miR-221 and miR-222 expression affects the proliferation potential of human prostate carcinoma cell lines by targeting p27Kip1 J. Biol. [score:5]
One of the HVT-encoded microRNAs, miR-H14-3p, showed close sequence identity to the chicken gga-miR-221 with perfect match of the 21/23 nucleotides including identical sequence of the seed region, suggesting that it is a virus-encoded ortholog [27]. [score:1]
There was also sequence homology between mdv1-miR-M31 and miR-221 in the seed region [37], but is limited to the nucleotide positions 2–7, corresponding to the minimal miRNA seed region. [score:1]
Similar to the miR-221 -mediated repression of p27 in cancer progression [60, 61], MDV-1 -induced tumorigenesis may also involve a similar mechanism [62]. [score:1]
Further evidence for this comes from the demonstration of partial sequence conservation between the downstream flanking region of hvt-miR-H14-3p in the HVT genome and the gga-miR-221 locus on chromosome 1 of the chicken genome. [score:1]
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[+] score: 20
In these two previous studies, the miRNAs gga-miR-221, gga-miR-211 and gga-miR-222a were found to be upregulated, whereas gga-miR-125b and gga-miR-193b were downregulated. [score:7]
According to our data, gga-miR-221, gga-miR-211 and gga-miR-222a were downregulated and gga-miR-125b and gga-miR-193b were upregulated in infected DCs compared with mock-infected DCs. [score:6]
The target genes of gga-miR-204, gga-miR-211, gga-miR-221 and gga-miR-6651 are involved in the processes indicated by the two GO terms. [score:3]
Based on these results, we found that antigen processing and presentation and apoptosis are significantly regulated by gga-miR-204, gga-miR-211, gga-miR-221 and gga-miR-6651. [score:2]
As shown in Fig. 4, gga-miR-221, gga-miR-125b, gga-miR-211, gga-miR-222a, gga-miR-193b, gga-miR-148a, gga-miR-27b, gga-miR-34a and gga-miR-130a were quantified by qRT-PCR, and these results were consistent with the sequencing analysis. [score:1]
gga-miR-221, gga-miR-222, gga-miR148, gga-miR-27b, gga-miR-34a and gga-miR-130a, which are related to differentiation and maturation, could also further influence the function of mature DCs. [score:1]
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[+] score: 18
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]
Starting with 16 known miRNAs validated as differentially expressed between broilers and layers, and eight muscle-related miRNAs (gga-miR-1, gga-miR-206, gga-miR-499, gga-miR-221, gga-miR-222, gga-miR-128, gga-miR-367 and gga-miR-27b), TargetScan (version 5.1) [43] was used to predict putative targets. [score:7]
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]
miRNAs with such variations from their miRBase reference sequences are referred to as isomiRs [34, 35]; some typical examples are presented in Figure 3. In the majority of cases (e. g. gga-miR-221) the most abundant isoform is identical to the reference in miRBase (Figure 3). [score:1]
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[+] score: 15
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]
Seven miRNAs (gga-miR-148a, gga-miR-101, gga-miR-100, gga-miR-92, gga-miR-130a, gga-miR-19a and gga-miR-221) with significantly differential expression levels were found (* P<0.05; ** P<0.01). [score:3]
Furthermore, we found that two miRNAs, gga-miR-92 and gga-miR-221, were significantly differentially expressed between the two chicken lines by qRT-PCR analyses. [score:3]
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[+] score: 14
Ectopic expression of miR-221 in differentiated myoblasts extended the cell cycle and delayed myogenin expression, which had a suppressive role on cell cycle inhibitor p27 [93]. [score:9]
Interestingly, miR-221 affected skeletal muscle cell growth and disease. [score:3]
Subsequently, we found that TGF-beta activated kinase 1/MAP3K7 binding protein 2 (TAB2) was target of gga-miR-221 using a luciferase reporter gene assay Fig. (2C and 2D). [score:2]
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[+] score: 14
Figure 3 shows that the expression of gga-miR-let 7, 199a-1, 26a, 181a, and -16 were all expressed at lower levels in tumors, compared to normal spleens, using either gga-miR-221 or U6 as a loading control; gga-miR-221 is slightly lower in tumors. [score:4]
In human, miR-221 and -222 are coordinately expressed from a single primary transcript [23]. [score:3]
We see about 1.7-fold higher abundance of ggg-miR-222 compared to gga-miR-221, consistent with their sharing a transcript that is highly expressed in CEF. [score:2]
Down regulation of p27Kip1 by miR-221/222 promotes growth and proliferation of cancer cells, and could play a similar role in dividing CEF [24]. [score:2]
These are located within a 3000 nt region of Chromosome 1, where there are two copies of gga-miR-222 followed by one copy of gga-miR-221. [score:1]
Frequently sequenced microRNAs include miR-221/222, which are thought to play a role in growth and proliferation. [score:1]
Blots were hybridized to gga-miR-221 to verify presence of microRNAs in each lane. [score:1]
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[+] score: 12
In vitro, gga-mir-221 and gga-mir-222 inhibit expression of CDK inhibitor protein p27/KIP1, but p27/KIP1 protein was increased in the MDV transformed lymphoblastoid cell line MSB-1 [88]. [score:7]
In our results gga-mir-221 was not differentially expressed and gga-mir-222a was decreased: and this is consistent with our data that p27/KIP1 protein is not differentially expressed. [score:5]
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[+] score: 12
MicroRNA signature in various cell types of mouse spermatogenesis: evidence for stage-specifically expressed miRNA-221, -203 and -34b-5p mediated spermatogenesis regulation. [score:4]
To date, several miRNAs, including gga-miR-221, gga-miR-222, gga-miR-23b, gga-miR-375, gga-miR-125b, gga-miR-1650, gga-miR-193a, gga-miR-193b, gga-let-7b, gga-let-7i, gga-miR-458, gga-miR-1456, gga-miR-1704, gga-miR-1777, gga-miR-1790, and gga-miR-2127, have been reported to be associated with tumorigenesis and the aberrant expression of the retrovirus, ALV-J (Li et al., 2012; Wang et al., 2013a, b; Li H. et al., 2014; Dai et al., 2015; Li et al., 2015). [score:3]
For example, four miRNAs (gga-miR-125b, gga-miR-193a, gga-miR-193b, and gga-miR-221) that are known to be involved in tumorigenesis-related pathways were shown to be expressed abnormally in ALV-J-infected chickens, and they might be associated with ALV-J -induced tumorigenesis (Wang et al., 2013a). [score:3]
Role of gga-miR-221 and gga-miR-222 during tumour formation in chickens infected by subgroup J avian leukosis virus. [score:1]
In addition, gga-miR-221, gga-miR-222, and gga-miR-375 have been shown to play a pivotal role in tumorigenesis after an ALV-J infection (Li H. et al., 2014; Dai et al., 2015). [score:1]
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[+] score: 10
Other miRNAs from this paper: gga-mir-155
miR-221 targets and suppresses the expression of a key cell cycle regulatory protein p27 [Kip1], which is involved in the induction and progression of T-cell lymphomas (Lambeth et al., 2009). [score:8]
Similar gene regulatory networks may be hijacked by miR-M31-3p, which shares a conserved seed homolog with miR-221 (Morgan et al., 2008). [score:2]
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[+] score: 9
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-24-1, hsa-mir-24-2, hsa-mir-25, mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-134, mmu-mir-137, mmu-mir-138-2, mmu-mir-145a, mmu-mir-24-1, hsa-mir-192, mmu-mir-194-1, mmu-mir-200b, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-215, hsa-mir-221, hsa-mir-200b, mmu-mir-296, mmu-let-7d, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-137, hsa-mir-138-2, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-134, hsa-mir-138-1, hsa-mir-194-1, mmu-mir-192, mmu-mir-200a, 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-24-2, mmu-mir-346, hsa-mir-200c, mmu-mir-17, mmu-mir-25, mmu-mir-200c, mmu-mir-221, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-200a, hsa-mir-296, hsa-mir-369, hsa-mir-346, mmu-mir-215, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-17, gga-mir-138-1, gga-mir-124a, gga-mir-194, gga-mir-215, gga-mir-137, gga-mir-7-2, gga-mir-138-2, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-200a, gga-mir-200b, gga-mir-124b, gga-let-7a-2, gga-let-7j, gga-let-7k, gga-mir-7-3, gga-mir-7-1, gga-mir-24, gga-mir-7b, gga-mir-9-2, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-192, dre-mir-221, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-7a-3, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-17a-1, dre-mir-17a-2, dre-mir-24-4, dre-mir-24-2, dre-mir-24-3, dre-mir-24-1, dre-mir-25, dre-mir-92b, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-137-1, dre-mir-137-2, dre-mir-138-1, dre-mir-145, dre-mir-194a, dre-mir-194b, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, mmu-mir-470, hsa-mir-485, hsa-mir-496, dre-let-7j, mmu-mir-485, mmu-mir-543, mmu-mir-369, hsa-mir-92b, gga-mir-9-1, hsa-mir-671, mmu-mir-671, mmu-mir-496a, mmu-mir-92b, hsa-mir-543, gga-mir-124a-2, mmu-mir-145b, mmu-let-7j, mmu-mir-496b, mmu-let-7k, gga-mir-124c, gga-mir-9-3, gga-mir-145, dre-mir-138-2, dre-mir-24b, gga-mir-9-4, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3, gga-mir-9b-1, gga-let-7l-1, gga-let-7l-2, gga-mir-9b-2
Mdm2 is negatively regulated by several miRNAs including miR-192 (Pichiorri et al., 2010), miR-194 (Pichiorri et al., 2010), miR-215 (Pichiorri et al., 2010), miR-221 (Kim et al., 2010), and miR-17 (Li and Yang, 2012) in different cellular contexts; however, whether these or other miRNAs regulate Mdm2 expression during the CNS development must be determined. [score:6]
MicroRNA-221 regulates chondrogenic differentiation through promoting proteosomal degradation of slug by targeting Mdm2. [score:3]
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[+] score: 9
gga-miR-221/222 suppresses the cell cycle of T-cell lymphoma in Marek's disease (MD) (Lambeth et al., 2009), and gga-miR-181a and gga-miR-26a inhibit proliferation of Marek's disease lymphoma cells (Li X. et al., 2014; Lian et al., 2015). [score:9]
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[+] score: 8
Other miRNAs from this paper: gga-mir-155, gga-mir-222a, gga-mir-222b
Previously, the miR-M31-derived mature miRNA miR-M31-3p has been shown to share a conserved seed sequence with miR-221 [33], which targets and suppresses a key cell cycle inhibitory regulator p27 [Kip1] protein, together with miR-222, in the induction and progression of T-cell lymphomas [34]. [score:8]
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[+] score: 7
In human cell lines, mir-200b was shown to inhibit the TLR4 pathway (Wendlandt et al., 2012), mir-221 increased the expression of NF-κβ and STAT3 (Liu et al., 2014), and mir-193b overexpression resulted in increased autophagy (Nyhan et al., 2016). [score:7]
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[+] score: 7
Four up-regulated miRNAs (gga-miR-221, gga-miR-30b, gga-miR-30c and gga-miR-215) and 1 down-regulated miRNA (gga-miR-375) in RSS chicken were chosen randomly to validate the Solexa sequencing results using RT-qPCR. [score:7]
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[+] score: 5
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-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-92a-1, hsa-mir-92a-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-140, hsa-mir-125b-2, hsa-mir-136, hsa-mir-146a, hsa-mir-150, hsa-mir-206, hsa-mir-155, hsa-mir-181b-2, hsa-mir-106b, hsa-mir-302a, hsa-mir-34b, hsa-mir-34c, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-125b-2, gga-mir-155, gga-mir-222a, gga-mir-92-1, gga-mir-19b, gga-mir-20a, gga-mir-19a, gga-mir-18a, gga-mir-17, gga-mir-16-1, gga-mir-15a, gga-mir-1a-2, gga-mir-206, gga-mir-223, gga-mir-106, gga-mir-302a, gga-mir-181a-1, gga-mir-181b-1, gga-mir-16-2, gga-mir-15b, gga-mir-140, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-146a, gga-mir-181b-2, gga-mir-181a-2, gga-mir-1a-1, gga-mir-1b, gga-let-7a-2, gga-mir-34b, gga-mir-34c, gga-let-7j, gga-let-7k, gga-mir-23b, gga-mir-27b, gga-mir-24, gga-mir-122-1, gga-mir-122-2, hsa-mir-429, hsa-mir-449a, hsa-mir-146b, hsa-mir-507, hsa-mir-455, hsa-mir-92b, hsa-mir-449b, gga-mir-146b, gga-mir-302b, gga-mir-302c, gga-mir-302d, gga-mir-455, gga-mir-367, gga-mir-429, gga-mir-449a, hsa-mir-449c, gga-mir-21, gga-mir-1458, gga-mir-1576, gga-mir-1612, gga-mir-1636, gga-mir-449c, gga-mir-1711, gga-mir-1729, gga-mir-1798, gga-mir-122b, gga-mir-1811, gga-mir-146c, gga-mir-15c, gga-mir-449b, gga-mir-222b, gga-mir-92-2, gga-mir-125b-1, gga-mir-449d, gga-let-7l-1, gga-let-7l-2, gga-mir-122b-1, gga-mir-122b-2
These results demonstrate that miRNA expression can be tissue-specific with high abundance of miR-221 and 222 in the CEF libraries and low abundances in lungs and tracheae. [score:3]
While both miR-221 and 222 had relatively lower abundance in the present study. [score:1]
Chicken miR-221 and miR-222, the most abundant miRNAs in the CEF small RNA libraries, had significantly higher reads in MDV infected than non-infected CEF [17]. [score:1]
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[+] score: 4
However, overlap between our data and zebra-fish cardiac enriched transcripts was limited to the miR499 and the miR133 family [26], while the Zebra fish cardiac enriched miR221 and miR130b miRNA transcripts showed significantly lower expression in our chicken heart data compared to embryo expression levels. [score:4]
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[+] score: 4
The SDE miRNAs with high fold-changes were all down-regulated in L30, including miR-146b-5p (−8.50-fold), miR-24-3p (−7.39-fold), miR-146a-5p (−5.96-fold), miR-221-5p (−5.85-fold), miR-7b (−5.35-fold), miR-147 (−5.11-fold), miR-20-5p (−4.59-fold), and miR-140b-5p (−4.57-fold). [score:4]
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[+] score: 4
We reported the involvement of several miRNAs including miR-34a [9, 10] and miR-221 [11] in JNK-regulated chondrogenic differentiation. [score:2]
Our laboratory also showed that JNK signaling is involved in the differentiation of chondroprogenitors in chicks through regulation of miR-34a [9, 10] and miR-221 levels [11]. [score:2]
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[+] score: 2
The regulation roles of miR-125b, miR-221 and miR-27b in porcine Salmonella infection signalling pathway. [score:2]
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[+] score: 1
MiR-221 and miR-222 have been found to be modulated during myogenesis and to play a role both in the progression from myoblasts to myocytes and in the achievement of the fully differentiated phenotype [28]. [score:1]
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