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14 publications mentioning gga-mir-101-1

Open access articles that are associated with the species Gallus gallus and mention the gene name mir-101-1. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 358
Other miRNAs from this paper: gga-mir-26a, gga-mir-21, gga-mir-101-2
Thus, it is reasonable to believe that the up-regulation of gga-miR-101-3p in the MG-infected chicken inhibits EZH2 expression, which in turn suppresses proliferation and cell cycle in chicken cells. [score:10]
To determine the roles of gga-miR-101-3p in regulation of EZH2 expression, we tested effects of over -expression or suppression of gga-miR-101-3p on EZH2 expression in DF-1 cells. [score:10]
Since it is well documented that miRNAs exert their function through regulating expression of their target gene(s) [45], we sought to identify the direct target of gga-miR-101-3p involved in MG-HS infection. [score:9]
Upon MG infection, gga-miR-101-3p expression in DF-1 cells was significantly up-regulated (Figure 7A), while EZH2 expression was significantly down regulated (Figure 7B). [score:9]
Subsequently, over -expression of miR-101-Inh drastically inhibited gga-miR-101-3p expression (Figure 4A), which, in turn, increased EZH2 expression at both mRNA and protein levels (Figure 4B,C). [score:9]
Thus, it is reasonable to believe that MG inhibits activation of MAPKs through up-regulation of gga-miR-101-3p and down-regulation of EZH2. [score:9]
As expected, a negative control for the gga-miR-101-3p specific inhibitor (miR-101-Inh-NC) did not inhibit EZH2 3′-UTR luciferase activity (Figure 2), which demonstrated that gga-miR-101-3p negatively regulated expression of EZH2 by binding to the complementary sequence in the 3′-UTR of EZH2 in a direct and sequence-specific manner. [score:9]
Lei Q. Shen F. Wu J. Zhang W. Wang J. Zhang L. miR-101, downregulated in retinoblastoma, functions as a tumor suppressor in human retinoblastoma cells by targeting EZH2 Oncol. [score:8]
During prostate cancer progression, miR-101 was down-regulated, and over -expression of miR-101 suppressed proliferation of prostate cancer cells [65, 66, 67]. [score:8]
One can imagine that the up-regulated gga-miR-101-3p would inhibit EZH2 expression, which, in turn, impairs T-cell function. [score:8]
An miRNA inhibitor sequences were as follows: gga-miR-101-3p inhibitor, 5′-UUCAGUUAUCACAGUACUGUAC-3′; random miRNA inhibitor negative control, 5′-CAGUACUUUUGUGUAGUACAA-3′. [score:7]
The data suggest that gga-miR-101-3p negatively regulates expression of EZH2 expression in DF-1 cells through binding to the 3′-UTR of EZH2. [score:6]
Ectopic expression of miR-101 significantly reduced cell growth and proliferation in retinoblastoma through directly targeting EZH2, which was associated with increased G1 phase arrest and cell apoptosis [71]. [score:6]
However, one can imagine that MG -induced up-regulation of gga-miR-101-3p in the lung tissues of chicken embryos may repress the expression of EZH2, which, in turn, prolong the activation of MAPKs, and increase tissue damage in hosts by MG infection. [score:6]
It is also reported that miR-101 inhibits lung cancer invasion through regulation of EZH2 [41], which inhibits cell proliferation and invasion, but enhances paclitaxel -induced apoptosis in non-small cell lung cancer [40]. [score:6]
Wang Y. Xiang W. Wang M. Huang T. Xiao X. Wang L. Tao D. Dong L. Zeng F. Jiang G. Methyl jasmonate sensitizes human bladder cancer cells to gambogic acid -induced apoptosis through down-regulation of EZH2 expression by miR-101 Br. [score:6]
In our study, gga-miR-101-3p was up-regulated in MG-infected SPF chicken embryos, which repressed the expression of EZH2. [score:6]
Over -expression of gga-miR-101-3p, but not miR-101-NC, resulted in a significant decrease of EZH2 expression at both mRNA and protein levels (Figure 3B,C). [score:5]
Taken together, these results indicate that over -expression of gga-miR-101-3p induces G1-phase arrest, which results in inhibition of cell growth and proliferation. [score:5]
The prediction software/servers from TargetScan [46], miRBase [22], miRecords [47], and miRDB [48] were used to search the putative protein-coding gene targets of gga-miR-101-3p. [score:5]
Zhang J. G. Guo J. F. Liu D. L. Liu Q. Wang J. J. MicroRNA-101 exerts tumor-suppressive functions in non-small cell lung cancer through directly targeting enhancer of zeste homolog 2 J. Thorac. [score:5]
Expression of luciferase can be inhibited by binding of gga-miR-101-3p to 3′-UTR of EZH2. [score:5]
Figure 3Over -expression of gga-miR-101-3p repressed EZH2 expression. [score:5]
Moreover, miR-101 is down-regulated in bladder transitional cell carcinoma, and directly represses EZH2 [68, 69]. [score:5]
The databases miRDB [48] and TargetScan [46] were used to search the target genes of gga-miR-101-3p. [score:5]
Figure 4Inhibition of gga-miR-101-3p increased EZH2 expression. [score:5]
Figure 5Over -expression of gga-miR-101-3p inhibited DF-1 cell proliferation. [score:5]
In the present study, we identified EZH2 as the target of gga-miR-101-3P and tested the effects of the miRNA on expression of EZH2 and cell growth in the context of MG infection. [score:5]
The miR-101 functions as a tumor suppressor in human retinoblastoma cells by targeting EZH2. [score:5]
The seed sequence of gga-miR-101-3p is underlined, and the complementary nucleotides between gga-miR-101-3p and EZH2 3′-UTR are indicated; (B) Secondary structure of the RNA duplex of gga-miR-101-3p and EZH2 3′-UTR target site (Red: Target sequence; Green: gga-miR101-3p); (C) Sequence alignment of EZH 2 3′-UTR from different species. [score:5]
Gga-miR-101-3p negatively regulates the expression of EZH2 gene by binding to complementary sequence in the 3′-UTR of EZH2. [score:4]
Consistent to our previous study, we found here that gga-miR-101-3p is up-regulated in MG-infected DF-1 cells and in the lung tissues of MG-infected chicken embryos. [score:4]
Cho H. M. Jeon H. S. Lee S. Y. Jeong K. J. Park S. Y. Lee H. Y. Lee J. U. Kwon S. J. Choi E. Na M. J. microRNA-101 inhibits lung cancer invasion through the regulation of enhancer of zeste homolog 2 Exp. [score:4]
Here, we observed that, upon MG infection, gga-miR-101-3p is up-regulated in the lung tissue. [score:4]
In our previous studies, we found that gga-miR-101-3p was up-regulated in the lungs of the infected chicken embryos by miRNA solexa sequencing (lab unpublished data). [score:4]
Liu L. Guo J. Yu L. Cai J. Gui T. Tang H. Song L. Wang J. Han F. Yang C. miR-101 regulates expression of EZH2 and contributes to progression of and cisplatin resistance in epithelial ovarian cancer Tumor Biol. [score:4]
Our preliminary study showed that gga-miR-101-3p was up-regulated in MG-infected SPF chicken embryos (lab unpublished data). [score:4]
EZH2 Is the Direct Target of gga-miR-101-3p. [score:4]
The miR-101 negatively regulates EZH2 in ovarian cancer cell lines, and miR-101 over -expression resulted in decreased cellular proliferation and migration [72]. [score:4]
Thus, we hypothesize that gga-miR-101-3p is involved in MG-infection through regulation of EZH2 expression. [score:4]
Figure 2EZH2 is the direct target of gga-miR-101-3p. [score:4]
Figure 7Effects of MG infection on the expression of gga-miR-101-3P and EZH2 in DF-1 cells. [score:3]
The duplex and the minimum free energy (mFE) between gga-miR-101-3p and 3′-UTR of the potential targets were analyzed by RNA hybrid [49]. [score:3]
Error bars represent the mean ± SD of triplicate experiments; (C) Transfection of miR-101-Inh increased protein expression of EZH2 in DF-1 cells. [score:3]
More importantly, we identified EZH2 as the target of gga-miR-101-3P. [score:3]
Figure 8Effects of MG infection on the expression of gga-miR-101-3P and EZH2 in the lungs of chicken embryos. [score:3]
Recent studies showed that miR-101 could target EZH2 in a variety of cancers. [score:3]
Both gga-miR-101-3p and EZH2 can be used as potential diagnostic biomarkers and therapeutic targets in treatment and prevention of MG infection. [score:3]
Effects of gga-miR-101-3p on EZH2 Expression. [score:3]
Expression of gga-miR-101-3p and EZH2 in MG-infected DF-1 Cells and Chicken Embryos. [score:3]
Wang H. J. Ruan H. J. He X. J. Ma Y. Y. Jiang X. T. Xia Y. J. Ye Z. Y. Tao H. Q. MicroRNA-101 is down-regulated in gastric cancer and involved in cell migration and invasion Eur. [score:3]
Prediction of the Target Gene of gga-miR-101-3p. [score:3]
As a negative control, miR-101-NC was over-expressed in DF-1 cells through transient transfection. [score:3]
Research has shown that miR-101 has been linked to tamoxifen and fulvestrant resistance by its targeting of EZH2 [73]. [score:3]
Figure 6Over -expression of gga-miR-101-3p arrested DF1 cells at G1 phase. [score:3]
Zhu Q. Y. Liu Q. Chen J. X. Lan K. Ge B. X. MicroRNA-101 targets MAPK phosphatase-1 to regulate the activation of MAPKs in macrophages J. Immunol. [score:3]
The predicted target site is at 94–114, with the seed region of miR-101 at 107-113 (Figure 1A). [score:3]
AmiGo [50] was used to analyze functions of the target genes of gga-miR-101-3p in Gallus gallus. [score:3]
Error bars represent the mean ± SD of triplicate experiments; (C) Western blot analysis of EZH2 protein expression in DF-1 cells transfected with gga-miR-101-3p. [score:3]
Figure 1Prediction of the target gene of gga-miR-101-3p. [score:3]
Huang F. Lin C. Shi Y. Kuerban G. MicroRNA-101 inhibits cell proliferation, invasion, and promotes apoptosis by regulating cyclooxygenase-2 in HeLa cervical carcinoma cells Asian Pac. [score:3]
Cao P. Deng Z. Wan M. Huang W. Cramer S. D. Xu J. Lei M. Sui G. Research MicroRNA-101 negatively regulates EZH2 and its expression is modulated by androgen receptor and HIF-1α/HIF-1β Mol. [score:3]
As expected, EZH2 expression showed opposite patterns as gga-miR-101-3p on the 10th–11th days of post-infection (equivalent to the 18th and 19th days of egg hatching) (Figure 8B). [score:3]
Friedman J. M. Liang G. Liu C. C. Wolff E. M. Tsai Y. C. Ye W. Zhou X. Jones P. A. The putative tumor suppressor microRNA-101 modulates the cancer epigenome by repressing the polycomb group protein EZH2 Cancer Res. [score:3]
When the gga-miR-101-3p specific inhibitor (miR-101-Inh) was transfected into the DF-1 cells, the luciferase activity was significantly increased even in the presence of gga-miR-101-3p. [score:3]
Through transient transfection, gga-miR-101-3p was over-expressed in DF-1 cells (Figure 3A). [score:3]
Data collection and analysis revealed that EZH2 was as a potential target gene of gga-miR-101-3p (score 98.36). [score:3]
The preliminary data showed that gga-miR-101-3P was up-regulated in the MG-infected lungs, compared with non-infected lungs, suggesting that gga-miR-101-3P may play an important role in MG infection of chicken. [score:3]
Predication of gga-miR-101-3p Target Genes. [score:3]
A number of studies have indicated that miR-101 is involved in a variety of diseases [40, 41, 42, 43, 44]. [score:3]
On the 9th–11th days of post-infection (equivalent to the 17th–19th days of egg hatching), we observed that gga-miR-101-3p expression was significantly higher in the lungs of the MG-infected chicken embryos than the non-infected group (Figure 8A). [score:3]
To further verify whether gga-miR-101-3p directly targets to the 3′-UTR of EZH2 in DF-1 cells, we performed a luciferase reporter assay. [score:3]
In the present study, we found that over -expression of gga-miR-101-3p leads to cell cycle arrest. [score:3]
Both miR-101 and EZH2 are highly conserved in many different species from chicken to human (Figure 1C), suggesting that miR-101-EZH2 is a common pathway in regulating immune response in vertebrates. [score:2]
The miRNA family of miR-101 play an important role for in regulating innate immune responses to infection. [score:2]
The DF-1 cells were transfected with gga-miR-101-3p or the negative control. [score:1]
A non-specific miRNA was used as a negative control for gga-miR-101-3p: sense 5′-UUCUCCGAACGUGUCACGUTT-3′ and antisense 5′-ACGUGACACGUUCGGAGAATT-3′. [score:1]
Cell proliferation assay showed that over -expression of gga-miR-101-3p significantly reduced the proliferation of DF-1 cells at 48 h and 72 h of post-transfection, compared to miR-101-NC or the blank control (Figure 5). [score:1]
On the 9th, 10th, and 11th days of post-infection, the lungs of the infected chicken embryos were processed and the expression of gga-miR-101-3p (A); and EZH2 (B) was measured by RT-qPCR. [score:1]
Then, we used RNAhybrid [49] to analyze the duplex and the minimum free energy (mFE between gga-miR-101-3p and EZH2 3’-UTR. [score:1]
DF-1 cells were transfected with gga-miR-101-3p or the negative control. [score:1]
To further explore the role of gga-miR-101-3p in MG-HS infection, we examined the effects of gga-miR-101-3p on DF-1 cell proliferation. [score:1]
Co-transfection of Luc-EZH2 (3′-UTR) with gga-miR-101-3p mimics (gga-miR-101-3p) in DF-1 cells resulted in a significant decrease of luciferase activity, while transfection of a non-specific RNA (miR-101-NC), did not affect luciferase activity (Figure 2). [score:1]
In DF-1 cells, gga-miR-101-3p significantly reduced the percentage of S-phase cells, but increased the percentage of G1-phase cells (Figure 6). [score:1]
DF-1 cells were transfected with gga-miR-101-3p or miR-101-NC, and then cultured for various periods of time (24 h, 48 h and 72 h). [score:1]
Since both miR-101 and EZH2 are highly conserved in a wide range of species (Figure 1C), the results obtained in chicken in this study will provide useful information and insights for the studies of other species. [score:1]
Next, we assessed the effects of gga-miR-101-3p on cell cycle distribution by flow cytometry. [score:1]
The gga-miR-101-3p mimics sequences was 5′-GUACAGUACUGUGAUAACUGAA-3′. [score:1]
Effects of gga-miR-101-3P on Cell Proliferation and Cell Cycle. [score:1]
Therefore, gga-miR-101-3p and EZH2 may be a privilege niche for MG to overcome the host immunity. [score:1]
To construct the dual luciferase reporter plasmid, the full length or the fragments of EZH2 3′-UTR covering the putative gga-miR-101-3P binding site were amplified by RT-PCR from the cDNA extracted from the lung tissues of chicken. [score:1]
Expression of gga-miR-101-3p and EZH2 was measured using RT-qPCR. [score:1]
[1 to 20 of 92 sentences]
[+] score: 166
Other miRNAs from this paper: gga-mir-34a, gga-mir-34b, gga-mir-34c, gga-mir-101-2
In conclusion, we demonstrate that miR-101 is downregulated in NPC, and can suppress NPC angiogenesis and metastasis in vitro and in vivo by targeting ITGA3. [score:8]
Quantitative RT-PCR and western blotting showed that the ITGA3 expression was markedly decreased in miR-101 -overexpressed NPC cells at both the mRNA and protein levels, while its expression was obviously increased in miR-101-knockdown cells, (Figures 3c and d). [score:8]
23, 24, 25, 26 It has been reported that miR-101 could inhibit migration and invasion by targeting AP-1 pathway in hepatoma cells, [27] and a more recent study shows that loss of miR-101 positively correlates with the upregulation of COUP-TFII activity, which contributes to prostate cancer metastasis. [score:8]
We observed that overexpression of miR-101 markedly reduced ITGA3 mRNA and protein expression, and the restoration of ITGA3 rescued the suppressive effects of miR-101 on NPC migration and invasion. [score:7]
To explore the mechanism by which miR-101 inhibit NPC angiogenesis and metastasis, we identified integrin subunit alpha 3 (ITGA3) as a potential target of miR-101 by TargetScan and miRanda (Figure 3a). [score:7]
Taken together, these data suggest that miR-101 is downregulated in NPC and there is a possible link between reduced miR-101 expression and NPC metastasis. [score:6]
Opposite to the function of miR-101, ITGA3 significantly promoted NPC cell migration and invasion, and ectopic expression of ITGA3 abrogated the inhibitory effects on migration and invasion induced by miR-101 in NPC cells (Figures 3h, i, k and l, P<0.01). [score:5]
In the present study, we confirmed that miR-101 was frequently downregulated in NPC cell lines and freshly frozen clinical samples; the same deregulation has also been observed by other groups. [score:5]
[22] Ectopic expression of miR-101 suppressed NPC cell migration, invasion and angiogenesis in vitro, while silencing of miR-101 promoted cell migration and invasion in vitro. [score:5]
However, depletion of endogenous miR-101 expression using miR-101 inhibitor markedly increased the migratory and invasive ability of HONE-1 and 6–10B cells (Figure 1d, both P<0.01). [score:5]
Furthermore, the expression of miR-101 was downregulated in cell lines with high metastatic potential (5–8F, S18) compared with cell lines with low metastatic potential (6–10B, S26) (Figure 1b; P<0.05). [score:5]
More importantly, we demonstrated that systemic administration of lentivirus -mediated miR-101 abrogated NPC lung metastatic ability in a mouse mo del without obvious toxicity, which provides a potent evidence for the development of a novel miRNA -targeting anticancer therapy. [score:4]
Next, vascular mimicry assay showed that 5–8F cells stably expressing lentivirus vector underwent a conspicuous rearrangement and formed a vasculogenic network within 22 h. In contrast, 5–8F cells stably overexpressing miR-101 showed a significant destruction of vascular mimicry structures and formed a significantly smaller total tube areas (Figure 1e, P<0.01). [score:4]
[21] Recently, our microarray analysis demonstrated that miR-101 was downregulated in NPC. [score:4]
In accordance with our previous microarray data, [15] quantitative RT-PCR confirmed that miR-101 was downregulated in 20 fresh-frozen NPC biopsy tissues compared with 16 normal nasopharyngeal epithelial tissues (Figure 1a, P<0.05). [score:3]
Taqman human Alu-specific PCR further validated that the number of cells metastasized to the lung with inoculated CAMs was much lower for miR-101 stably overexpressing group than controls (Figure 2f, P<0.05), which indicated a diminished intravasation and metastatic ability. [score:3]
29, 30 In our mouse NPC lung metastatic mo del, we did observe that the systemic delivery of lent-miR-101 exhibited a high infectious efficiency and a high expression level of miR-101 in the lungs of mice without obvious toxicity, demonstrating lentivirus as an effective and non-toxic means to deliver miRNAs to mouse. [score:3]
In our present study, we identified ITGA3 as a potential target of miR-101 using two open-access databases. [score:3]
Furthermore, we evaluated the expression level of miR-101 in NPC cell lines, and confirmed that miR-101 was downregulated in all of the 10 tested NPC cell lines compared with two immortalized nasopharyngeal epithelial cell lines (Figure 1b). [score:3]
Systemic delivery of miR-101 suppresses lung metastasis in NPC mouse mo del. [score:3]
[28] These data suggest a powerful tumour suppressive activity of miR-101 in human cancers. [score:3]
Based on the demonstration of the function and mechanism of miR-101 involved in NPC metastasis, we further tested the hypothesis that miR-101 could serve as a therapeutic target for NPC In this study, we chose a lentivirus -based system as miR-101 administration vehicle, since its safety has been tested in preclinical research and clinical trials and it could provide a therapeutic benefit for the patients. [score:3]
Moreover, miR-101 expression was much lower in primary NPC tissues with high level regional lymph node metastasis than those with low level regional lymph mode metastasis (Figure 1a, P<0.05). [score:3]
Moreover, hematoxylin and eosin (H&E) staining showed that control 5–8F cells that were implanted onto the CAM invaded into the connective tissues through the breached basement membrane, while cells stably overexpressing miR-101 failed to invade the basement membrane (Figure 2c). [score:3]
More importantly, systemic delivery of lent-miR-101 suppressed the formation of metastatic nodules in lungs of mice. [score:3]
In addition, fewer tumour cell nests were present in the chorioallantoic mesenchymal in the miR-101 stably overexpressing group (Figure 2d), and immunohistochemistry staining of cytokeratin CKAE1/3 confirmed the epithelial origin of micro-tumours (Figure 2e). [score:3]
Luciferase reporter assay showed that the luciferase activity of the wild-type ITGA3 3′ UTR reporter gene was significantly reduced in CNE-2 and 5–8F cells transfected with miR-101 mimic, whereas the mutant reporter gene was not affected (Figure 3b, P<0.01), which confirmed that ITGA3 is a direct target of miR-101. [score:3]
These results validate that the invasive behaviour of NPC could be suppressed by miR-101 administration. [score:3]
MiR-101 is downregulated in NPC clinical specimens and cell lines. [score:3]
ITGA3 is a functional target of miR-101 in NPC. [score:3]
Cells were also co -transfected with miR-101 mimic or miR-Ctrl and either the empty vector control (Vector) or pEZ-Lv105-ITGA3 (ITGA3) plasmid overexpressing ITGA3 (FulenGen, Guangzhou, China) using Lipofectamine 2000 reagent. [score:3]
miR-101 mimic, inhibitor and their corresponding controls (GeneParma, Suzhou, China) were transfected into NPC cells using Lipofectamine 2000 reagent (Invitrogen). [score:3]
These results suggest that miR-101 can suppress the migratory, invasive and angiogenic ability of NPC cells in vitro. [score:3]
The CAM data further indicate that miR-101 inhibits the ability of angiogenesis, intravasation and metastasis of NPC cells in vivo. [score:3]
MiR-101 inhibits NPC cell angiogenesis and metastasis in a CAM mo del in vivoThe in vitro results led us to examine the effect of miR-101 on NPC cell angiogenesis and metastasis in vivo using the chick chorioallantoic membrane (CAM) assay. [score:2]
MiR-101 suppresses NPC cell migration, invasion and angiogenesis in vitro. [score:2]
Next, using luciferase reporter assays, we validated ITGA3 as a novel target of miR-101. [score:2]
As shown in Figure 2a, a markedly reduced number of blood vessels formed in the miR-101 stably overexpressing group compared with mock and lentivirus vector control groups, which was further validated by quantification analysis (Figure 2b, P<0.01). [score:2]
Moreover, our CAM data strongly implicated that miR-101 was involved in regulating NPC tumour invasion and metastasis through its activity in tumour cell intravasation, extravasation and subsequent cell seeding. [score:2]
MiR-101 inhibits NPC cell angiogenesis and metastasis in a CAM mo del in vivo. [score:2]
[7] MiR-101 has many validated oncogenic targets, including FOS, EZH2, MCL-1 and ROCK2. [score:2]
The pri-miR-101 sequence was cloned into the lentiviral plasmid pSin-EF2-puromycin (Addgene, Cambridge, MA, USA); pSin-EF2-miR-101-coGFP or negative control pSin-EF2- coGFP vector was then co -transfected into 293FT cells with the psPAX2 packaging plasmid (Addgene) and the pMD2. [score:1]
As for the treatment effect, the number of macroscopic and microscopic metastatic nodules formed in the lung tissues of lent-miR-101 mice group was remarkably smaller than the lent-miR-ctrl mice group (Figures 5c–f, both P<0.01). [score:1]
Due to the effective role of miR-101 in the inhibition of NPC metastasis and angiogenesis, we then evaluated the therapeutic efficacy of miR-101 in a mouse mo del of lung metastasis. [score:1]
After 2 weeks, lentivirus-miR-101-coGFP (lent-miR-101), or lentivirus-miR-ctrl-coGFP (lent-miR-ctrl) were injected via tail vein at a dose of 10 [8] MOI per mouse (200 μl) using a 30-gauge ultra-fine insulin syringe two times a week for a month. [score:1]
Notably, no acute liver toxicity and other organ toxicity were observed in mice after the delivery of lent-miR-101 or lent-miR-ctrl, which were determined by histological dissection (Figure 5g) and serological markers (Figure 5h). [score:1]
As shown in Figure 5a, the levels of coGFP in the lung tissues of lent-miR-101 or lent-miR-ctrl treated mice were similar, exhibiting a high infectious efficiency, while the levels of miR-101 in the lung tissues of lent-miR-101 treated mice were significantly higher than control mice (Figure 5b, P<0.01). [score:1]
Overall, our data hereby provide a basis for the concept that the systemic administration of miR-101 mediated by lentivirus might be a clinically viable anti-NPC therapeutic strategy. [score:1]
U6 or GAPDH were used as endogenous controls for miR-101 and ITGA3, respectively, and the relative expression was calculated with the 2 [−ΔΔCT] equation. [score:1]
Furthermore, CNE-2 and 5–8F cells were co -transfected with miR-101 mimic or miR-ctrl and either the empty vector or pEZ-Lv105-ITGA3 plasmid, which encoded the full-length coding sequence of ITGA3 without its 3′ UTR (Figures 3g and j). [score:1]
Two weeks after the preparation of the lung colonization mo del, lent-miR-ctrl or lent-miR-101 was, respectively, administered to mice via tail vein two times a week for a month. [score:1]
Systemic administration of lenti-miR-101 to a lung metastasis mouse mo del. [score:1]
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[+] score: 97
These results indicate that similar responses are likely to be happening in the host during SE infection, that is, the down-regulation of gga-miR-101-3p may result in increased expression of IRF4 during Salmonella infection, and up-regulation of gga-miR-155 may inhibit expression of LRRC59. [score:13]
The results showed that miR-155 overexpression markedly decreased the expression of IL-6 and TNF-α compared with control miRNA or miR-155 inhibitor (Figure 7A; P < 0.01), while miR-101 knockdown significantly decreased the expression of IL-6 and TNF-α compared with control miRNA inhibitor (Figure 7B; P < 0.05). [score:10]
In addition, gga-miR-101-3p directly inhibited IRF4 expression and miR-101- KO significantly decreased the expression of IL-6 and TNF-α compared with control miRNA inhibitor (P < 0.05). [score:9]
Two miRNAs, gga-miR-155 and gga-miR-101-3p, could directly alter the expression of target IRF4 and LRRC59 and regulate the production of pro-inflammatory cytokines, respectively. [score:7]
The expression of gga-miR-101-3p was significantly down-regulated in S vs. [score:6]
After 36-h treatment with mimic, elevating gga-miR-155 significantly repressed the mRNA expression levels of LRRC59 compared to the miR-NC and negative controls (P < 0.05); In contrast, after 36-h treatment with gga-miR-101-3p inhibitor, the mRNA expression levels of IRF4 were significantly increased (P < 0.05) compared to the controls (Figure 6). [score:5]
Although, the expression levels of miR-101-3p were relatively moderate, it is highly connected (>8 SE-related target genes) within the miRNA-mRNA network. [score:5]
Based on the foregoing observations and interpretations, it is reasonable to propose that gga-miR-155 and gga-miR-101-3p contribute to SE -induced pathogenesis and regulate the production of pro-inflammatory cytokines through directly down -regulating LRRC59 and up -regulating IRF4 genes, respectively. [score:5]
Figure 7Gga-miR-155 and gga-miR-101-3p regulate expression of pro-inflammatory cytokine genes induced by LPS. [score:4]
The pmiR-RB-Report™ (RiboBio, Guangzhou, China) including double luciferase reporter genes was used to test and validate the target sites for gga-miR-155 and gga-miR-101-3p. [score:3]
The present study of splenic miRNA and mRNA profiles from chickens after Salmonella challenge has identified differential expression of several miRNAs linked to immune responses, including miR-155, miR-9, miR-30 which have been reported previously and several miRNAs, such as miR-101-3p and miR-130b-3p, which were shown here to be associated with the immune response to infection with SE. [score:3]
Over-expressed gga-miR-155 and interference gga-miR-101-3p in chicken HD11 macrophage cells. [score:3]
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]
To further validate the biological function of gga-miR-155 and gga-miR-101-3p in a chicken macrophage-like line HD11, 100 μM mimic (gga-miR-155), inhibitor (gga-miR-101-3p) and control oligos (gga-miR-NC) were transfected into HD11 cells using 12-well plates and TransIT®-2020 (Mirus Bio, Madison, WI) per the manufacturer's instructions. [score:3]
These data demonstrate that gga-miR-155 and gga-miR-101 could regulate the production of pro-inflammatory cytokines, IL-6 and TNF-a, which may play a negative role in response to LPS stimulation in chickens. [score:2]
IFR4 was predicted to be regulated by gga-miR-30d and gga-miR-101-3p. [score:2]
One Salmonella-regulated miRNA of particular interest identified through the present study is gga-miR-101-3p. [score:2]
Figure 4Regulation of IRF4 by gga-miR-101-3p. [score:2]
In order to address the effect of miR-155 and miR-101 on the induction of pro-inflammatory cytokines in response to LPS, the expression levels of IL-6 and TNF-α were measured in a macrophage inflammatory response mo del. [score:1]
Validations of miRNA-mRNA interactions using gga-miR-101-3p- IRF4 and gga-miR-155- LRRC59 mimics. [score:1]
The 3′ UTRs of IRF4 and LRRC59 were cloned into luciferase reporter plasmids to test gga-miR-101-3p and gga-miR-155 functions in vitro. [score:1]
In contrast, gga-miR-101-3p has not been previously linked to Salmonella infection; the present finding in chicken spleen is novel. [score:1]
Figure 6Validations of biological function of gga-miR-155 and gga-miR-101-3p in chicken HD11 macrophages. [score:1]
The 3′ UTR of IRF4 and LRRC59 containing gga-miR-101-3p and gga-miR-155 binding sites were amplified from chicken genomic DNA. [score:1]
Since hub nodes have been found to play important roles in many networks (He and Zhang, 2006), the presence of hub miRNAs was sought and, several were identified including gga-miR-155 and gga-miR-101-3p (Figure 3). [score:1]
Validations of biological function of gga-miR-155 and gga-miR-101-3p in chicken HD11 macrophage cells. [score:1]
Validations of miRNA-mRNA interactions using gga-miR-101-3p- IRF4 and gga-miR-155- LRRC59 mimicsThe luciferase reporter gene system was used to validate the above-stated predicted interactions. [score:1]
When the cells reached 70 to 80% confluence, pmiR-3′ UTR (100 ng) was co -transfected with 50 nM of a negative control or a gga-miR-101-3p mimic (GenePharma, Shanghai, China) using 0.30 μL of FugeneHD (Promega, Madison, WI) according to the manufacturer's instructions. [score:1]
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[+] score: 32
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]
Last but not least, expression levels of 10 miRNAs can be perturbed in animals when fed with high-fat diet (miR-142–5p and miR-101) [74– 78], or with obesity or obesity-related diseases (miR-10a, miR-218, miR-429, miR-200a, miR-200b, miR-451, miR-142–3p, and miR-454) [77, 79– 85], which indicates that they could be potentially related to adipogenesis. [score:5]
After qRT-PCR analyses, gga-miR-101 was also found to be significantly differentially expressed, and gga-miR-1a and gga-miR-17–3p were suggestively significant. [score:3]
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]
Four miRNAs significantly differentially expressed between the fat and lean chicken lines detected by deep sequencing were included in the list, i. e. gga-miR-101, gga-miR-2188, gga-miR-1a and gga-miR-17–3p. [score:3]
Among the 33 significantly differentially expressed miRNAs, gga-miR-101 had the largest number of reads in both fat and lean lines. [score:3]
With the highest number of reads in both chicken lines among the significantly differentially expressed miRNAs, miR-101 was found previously to be able to induce the differentiation of 3T3-L1 [60]. [score:3]
Some miRNAs such as gga-miR-101 and gga-miR-1a were significantly differentially expressed between the fat and lean chicken lines. [score:3]
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[+] score: 23
Therefore, although little is known about the specific functions of several of these miRNAs (e. g. miR-31, miR-101, miR-200b, miR-10b, miR-460, miR-15b, miR-16 and miR203) during muscle development, the close relationship between their targets and myogenesis regulation demonstrates a potential role during muscle development. [score:6]
Seven (miR-101, miR-10a, miR-10b, miR-1677, let-7f, miR-31, and miR-205b) were expressed at higher levels in layers, and ten (miR-203, miR-200b, miR-16c, miR-15b, miR-15c, miR-460, miR-429, let-7c, miR-2188, and gga-miR-N2) were expressed at higher levels in broilers. [score:5]
No miRNAs have been identified previously as regulatory factors for ACVR2B, but the network analysis predicted that ACVR2B is a target of three miRNAs: gga-miR-101, gga-miR-1a and gga-miR-499 (Figure 6B). [score:4]
However, the majority including one novel miRNAs (gga-miR-N2) and eight known miRNAs (miR-101, miR-15b, miR-15c, miR-1677, miR-200, miR-460, gga-mir-2188 and miR-429) have not been implicated in the regulation of muscle development. [score:3]
The interaction networks predicted that ACVR2B is a target of gga-miR-101, gga-miR-1a and gga-miR-499. [score:3]
Little is known about the functional roles of the remaining eight (miR-31, miR-101, miR-200b, miR-10b, miR-460, miR-15b, miR-16 and miR-203) during muscle development. [score:2]
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[+] score: 18
In this study, gga-miR-101 was abundantly expression in chicken ovary and 123 putative target genes were involved in TGF-β signaling pathway. [score:5]
Bioinformatic analysis shows that miR-101 targets TGIF1 (TGFB -induced factor homeobox 1), ZEB2 (zinc finger E-box binding homeobox 2) and BMPR1B, which participate in the regulation of TGF-β signaling [56]. [score:4]
The following 15 miRNAs were dominantly expressed in the two libraries: gga-miR-10a, gga-miR-146c, gga-miR-101, gga-miR-21, gga-let-7a, gga-let-7b, gga-let-7c, gga-let-7j, gga-let-7f, gga-let-7 k, gga-miR-30a-5p, gga-miR-30e, gga-miR-148a, gga-miR-100 and gga-miR-126. [score:3]
The increase in female miR-101 expression in differentiating ovaries can ease repression of TGF-β signaling [60]. [score:3]
Studies indicated that gga-miR-31, gga-miR-101, gga-miR-202 and gga-miR-202* may be involved in regulating gonadal differentiation in embryonic chicken gonads [54- 56]. [score:2]
Furthermore, gga-miR-101, gga-miR-1a, gga-miR-146c, gga-miR-148a, gga-miR-126, gga-miR-26a and gga-miR-30d were abundant in our sequencing libraries, as has been shown in other animal gonads [25, 27, 28]. [score:1]
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[+] score: 17
In summary, miRNAs, such as miR-101,play an indispensable role in establishing certain organs by localizing or fast shifting expression in appropriate timing with embryonic development. [score:4]
Although three miRNAs, miR-1, miR-101, and miR-499, were predicted to target the activin A receptor type IIB (ACVR2B) gene, validation was only performed for miR-1 and ACVR2B. [score:3]
It is likely that the high abundance of miR-101 after gonadal differentiation in females is crucial for determining the nature of ovarian cells due to its inhibitory effect on SRY (sex determining region Y)-box 9 (SOX9), a key component of testes differentiation. [score:3]
Expression patterns of 15 miRNAs identified using RT-PCR agreed with those identified using deep sequencing, miR-101, miR-10a, miR-10b, miR-1677, let-7f, and miR-31 were higher in layers, while miR-200b, let-7c, miR-16c, miR15b, miR-15c, miR460, miR-429, miR-2188, and the novel miR-N2 were higher in broilers. [score:3]
miR-101 may monitor gonadal development to determine the gender of a chicken [84]. [score:2]
In males, miR-101 may be responsible for testes formation by fine tuning SOX9. [score:1]
Many growth-related miRNAs have been discovered, including miR-1, miR-133, miR-206, miR-101, and let-7b, the biochemical roles of which have been demonstrated through experimental validation. [score:1]
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[+] score: 14
In addition, SERPINB3 3′-UTR mutants including mutated binding sites for miR-101, miR-1668 and miR-1681 were also generated by point mutation in order to confirm the modulation of eGFP expression by each miRNA (Figure 3B). [score:4]
In the presence of miR-101, miR-1668 and miR-1681, the intensity and percentage of GFP -expressing cells (44.8% in control vs. [score:3]
For the dual fluorescence reporter assay, the fusion constructs containing the DsRed gene and either miR-101, miR-1668 and miR-1681 were designed to be co-expressed under control of the CMV promoter (pcDNA-DsRed-miRNA). [score:2]
[A] Diagram of miR-101, miR-1668 and miR-1681 binding sites in SERPINB3 3′-UTR. [score:1]
27.5% in miR-101, 24.2% in miR-1668, 14.8% in miR-1681) decreased (p<0.01). [score:1]
16.1% in miR-101, 13.5% in miR-1668, 14.3% in miR-1681) as a control (Figure 3D). [score:1]
org/miRDB/) revealed three putative binding site for miR-101, miR-1668 and miR-1681 (Figure 3A). [score:1]
[C] After co-transfection of pcDNA-eGFP-3′UTR for the SERPINB3 transcript and pcDNA-DsRed-miRNA for the miR-101, miR-1668 and miR-1681, the fluorescence signals of GFP and DsRed were detected using fluorescent microscopy. [score:1]
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[+] score: 8
MiR-101-3p (−2.1-fold) and miR-15c-5p (−1.4-fold) had the most target genes followed by miR-15a, miR-16-5p, miR-214, miR-16c-5p, and miR-181b-5p (Supplementary Table S4), and these miRNAs were all down-regulated in L30 compared with L20. [score:5]
These two genes were targeted by the highest numbers of miRNAs, including miR-101-3p and miR-21-3p. [score:3]
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[+] score: 7
Other miRNAs from this paper: hsa-mir-101-1, hsa-mir-101-2, gga-mir-101-2
It was reported that the inhibition of EZH2 may be a potential therapeutic strategy to target GBM proliferation, migration, and angiogenesis as the inhibition of EZH2 in vitro by pre-miR-101, EZH2 siRNA, or small molecule DZNep attenuated GBM cell growth, migration/invasion, and GBM -induced endothelial tubule formation in a U87-Fluc-mCherry GBM xenograft mouse imaging mo del resulted in a reduced tumor growth and migration/invasion. [score:7]
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[+] score: 6
Other miRNAs from this paper: gga-mir-217, gga-mir-101-2
Moreover, MALAT-1 inhibited proliferation, migration and invasion of esophageal squamous cell carcinoma cells via regulation of the expression of miR-101 and miR-217 [18]. [score:6]
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[+] score: 5
Our previous study has shown that gga-miR-101-3p plays a crucial role in MG infection by regulating EZH2 expression (Chen et al., 2015). [score:4]
gga-miR-101-3p plays a key role in Mycoplasma gallisepticum (HS strain) infection of chicken. [score:1]
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[+] score: 3
Ten mature miRNAs with the highest expression comprised approximately 50% of all miRNAs, showing a relatively abundant distribution (Fig.   5D), while miR-21, miR-26a, miR-125b, miR-101, and miR-199 were the most abundant miRNAs overall, together accounting for 33% of the total. [score:3]
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[+] score: 2
Other miRNAs from this paper: gga-mir-101-2
Kottakis F. Polytarchou C. Foltopoulou P. Sanidas I. Kampranis S. C. Tsichlis P. N. FGF-2 regulates cell proliferation, migration and angiogenesis through an NDY1/KDM2B-miR-101-EZH2 pathway Mol. [score:2]
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