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6 publications mentioning hsa-mir-1269b

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-1269b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 289
Indeed, FOXO1 expression was found to be downregulated in the miR-1269 -overexpressing BEL-7404 and Huh7 cells but upregulated in the cells transfected with miR-1269 inhibitor. [score:13]
In the present study, we found that FOXO1 is a direct target of miR-1269, which could downregulate its expression. [score:9]
As expected, p21 [Cip1] was upregulated, whereas cyclin D1 and phosphorylated Rb were downregulated, in miR-1269 -inhibitor transfected cells (Figure  4E and F). [score:9]
Importantly, western blotting analysis showed that FOXO1 expression was downregulated in the eight pairs of HCC tissue, compared with the adjacent noncancerous hepatic tissues, and statistical analysis revealed that miR-1269 levels inversely correlated with the expression of FOXO1 in the clinical HCC samples (Figure  4B), suggesting that miR-1269 might play role in regulation of FOXO1 in HCC. [score:8]
These results further confirm that miR-1269 enhances HCC cell proliferation and tumorigenicity by downregulation of FOXO1 expression, and that FOXO1 suppression is essential for miR-1269 -mediated effects on HCC cell proliferation and tumorigenicity. [score:8]
Consistent with this literature, we found that ectopic miR-1269 inhibits the expression of p21 [Cip1], and induces the expression of cyclin D1. [score:7]
In addition, overexpressing miR-1269 decreased the expression of p-FOXO1, but we did not found significant alterations of FOXO1 in miR-1269 -inhibited cells (Figure  4C). [score:7]
As shown in Figure  4E and F, p21 [Cip1] was downregulated, but cyclin D1 and phosphorylated Rb, were upregulated in miR-1269 -transfected cells. [score:7]
Suppression of FOXO1 by miR-1269 was associated with dysregulation of p21, cyclin D1, phosphorylated Rb and Ki67 expression, thereby playing an essential role in the growth of HCC cells. [score:6]
To further confirm the effect of FOXO1 suppression on miR-1269 -mediated proliferation of HCC cells, siRNA assay was used to suppress endogenous FOXO1 expression (Figure  5A). [score:6]
In conclusion, our results indicated that overexpression of miR-1269 could promote cell proliferation, tumorigenicity and cell cycle progression in HCC by directly suppressing FOXO1. [score:6]
Our study indicated that overexpression of miR-1269 promotes cell proliferation in HCC through directly suppressing FOXO1, and functions as an oncomiR in HCC. [score:6]
The colony formation and anchorage-independent growth assays both showed that silencing FOXO1 expression could reverse the inhibitory effect of the miR-1269 inhibitor on HCC cell proliferation (Figure  5C and D). [score:6]
Furthermore, we demonstrated that the tumor suppressor gene FOXO1 is a direct target of miR-1269. [score:6]
Inhibition of miR-1269 suppresses proliferation of HCC cells. [score:5]
Taken together, these results suggest that inhibition of miR-1269 suppresses the proliferation, tumorigenicity and cell cycle progression of HCC cells. [score:5]
Thus, we used publicly available algorithms (TargetScan 6.2) to predict the potential targets of miR-1269. [score:5]
Ectopic miR-1269 expression promoted, but inhibition of miR-1269 reduced, proliferation, tumorigenicity and cell cycle progression of HCC cells. [score:5]
Figure 3 Inhibition of miR-1269 suppresses the proliferation and tumorigenicity of HCC cells. [score:5]
Meanwhile, mutant miR-1269 failed to show an inhibitory effect on luciferase expression driven by the pGL3- FOXO1 -3’-UTR-luciferase reporter (Figure  4D). [score:5]
Figure 4 FOXO1 is a direct target of miR-1269. [score:4]
was used to determine whether FOXO1 is the direct target of miR-1269. [score:4]
miR-1269 was upregulated in HCC cells and tissues. [score:4]
Collectively, these results suggest that upregulation of miR-1269 enhanced the proliferation, tumorigenicity and cell cycle progression of HCC cells. [score:4]
FOXO1 is a direct target of miR-1269 in HCC cells. [score:4]
Analysis by MTT assay indicated that suppression of FOXO1 in cells transfected with the miR-1269 inhibitor increased the growth rate of HCC cells (Figure  5B). [score:4]
showed that upregulation of miR-1269 promoted the colony formation capacity of BEL-7404 and Huh7 cells (Figure  2C). [score:4]
Collectively, these results suggest that miR-1269 directly targets FOXO1 in HCC cells. [score:4]
In the current study, we found that miR-1269 was upregulated through analysis of a published micro-array -based high-throughput assessment (NCBI/GEO/GSE36915), and further confirmed this result in HCC tissue and cell lines. [score:4]
Analysis by MTT assay showed that downregulation of miR-1269 markedly decreased the growth rate of BEL-7404 and Huh7 HCC cells transfected with the miR-1269 inhibitor, compared with that of control cells (Figure  3B). [score:4]
Furthermore, we demonstrated that FOXO1 was a direct target of miR-1269. [score:4]
The luciferase assay results showed that ectopic overexpression of miR-1269 decreased, but inhibition of miR-1269, increased luciferase activity of the pGL3- FOXO1-3’-UTR reporter (Figure  4D). [score:4]
A. Real-time PCR analysis miR-1269 in BEL-7404 and Huh7 cells transfected with a miR-1269 inhibitor. [score:3]
The miR-1269 expression plasmid was generated by cloning the genomic pre-miR-1269 gene into the retroviral transfer plasmid pMSCV-puro (Clontech Laboratories, Mountain View, CA, USA). [score:3]
The miR-1269 mimic, miR-1269 mutant mimic (miR-1269-mut), miR-1269 inhibitor, negative control (NC) and FOXO1 siRNA were purchased from RiboBio (RiboBio, Guangzhou, Guangdong, China). [score:3]
Ectopic overexpression of miR-1269 in HCC cell lines led to the promotion of cell growth rate, tumorigenicity and cell cycle progression. [score:3]
To explore the biological function of miR-1269 in HCC progression, BEL-7404 and Huh7 cells stably overexpressing miR-1269 were established (Figure  2A). [score:3]
This work adds to the growing body of knowledge concerning the essential role that miRNAs play in the pathogenesis of cancer, and further suggests that miR-1269 is an oncomiR and might represent a potential therapeutic target for HCC. [score:3]
A. Real-time PCR analysis of miR-1269 in BEL-7404 and Huh7 cells stably overexpressing miR-1269. [score:3]
D. The FOXO1 luciferase reporter activity in the indicated cells transfected with miR-1269 mimic, or miR-1269-mut, miR-1269 inhibitor, or negative control. [score:3]
Figure 1 MiR-1269 is upregulated in HCC. [score:3]
Moreover, we found that miR-1269 was also upregulated in eight HCC cell lines (Hep3B, HepG2, BEL-7402, BEL-7404, MHCC97H, MHCC97L, Huh7, and QGY-7703), compared with that in the normal liver epithelial cell line THLE3 cells and normal hepatocytes (Normal) (Figure  1C). [score:3]
B. Real-time PCR analysis of miR-1269 expression in 23 paired cancerous tissues (T) and their adjacent noncancerous hepatic tissues (ANT). [score:3]
To further confirm the direct regulation of FOXO1 by miR-1269, the pGL3- FOXO1-3’-UTR-luciferase reporter, containing the three putative miR-1269 binding sites, was constructed. [score:3]
As shown in Figure  1B, miR-1269 was upregulated in all 23 pairs of HCC tissue, compared with the adjacent noncancerous hepatic tissues. [score:3]
To further explore the role of miR-1269 in promoting HCC cell proliferation, loss of function approach using a miR-1269 inhibitor were performed (Figure  3A). [score:3]
Suppression of FOXO1 is essential for miR-1269 -induced cell proliferation in HCC. [score:3]
We further examined the expression level of miR-1269 in HCC tissues and cell lines by qRT-PCR. [score:3]
A shown in Figure  2B, ectopic expression of miR-1269 increased the growth rate of both HCC cell lines. [score:3]
MiR-1269 is upregulated in HCC tissues and cells. [score:3]
Ectopic overexpression of miR-1269 promotes proliferation of HCC cells. [score:3]
A. miR-1269 is upregulated in HCC tissues compared with normal liver tissue (P = 0.015; NCBI/GEO/ GSE36915). [score:3]
Furthermore, cell cycle analysis by flow cytometry showed a dramatic decrease in the percentage of cells in the G1/G0 phase and an increase in the percentage of cells in the S phase in miR-1269 -overexpressing cells (Figure  2E). [score:3]
The expression of miR-1269 in HCC cells and tissues were determined by Real-time PCR analysis. [score:3]
Taken together, these data demonstrate that miR-1269 expression is elevated in HCC tissues and cell lines. [score:3]
By analyzing a published micro-array -based high-throughput assessment (NCBI/GEO/GSE36915; n (Non-tumor) = 21; n (Tumor) =68), miR-1269 was found to be significantly upregulated in HCC tissues, compared with that in non-tumor tissues (P < 0.05; Figure  1A). [score:3]
B. The effects of miR-1269 inhibition on cell viability of the indicated cell lines analyzed by MTT assay. [score:2]
B. The effects of miR-1269 overexpression on cell viability of the indicated cell lines analyzed by MTT assay. [score:2]
These results suggest that miR-1269 plays an important role in the proliferation of HCC cells via regulation of FOXO1. [score:2]
Moreover, the result of flow cytometry showed an obvious increase in the percentage of cells in the G1/G0 phase and a decrease in the percentage of cells in the S phase in miR-1269 inhibited cells, compared with control cells (Figure  3E). [score:2]
The colony formation and anchorage-independent growth assays both revealed that HCC cells transfected with the miR-1269 inhibitor produced fewer and smaller colonies than the NC cells (Figure  3C and D). [score:2]
D. Effects of miR-1269 inhibition on the tumorigenicity of the indicated cell lines determined by anchorage-independent growth ability assay. [score:2]
Figure 5 MiR-1269 promotes proliferation of HCC cells by suppressing FOXO1. [score:2]
Consistently, anchorage-independent growth assay revealed that the cells stably expressing miR-1269 formed more and larger-sized colonies than the control cells (Figure  2D). [score:2]
C. Real-time PCR analysis of miR-1269 expression in several HCC cell lines compared to normal hepatic cells as control. [score:2]
However, the function and regulation of miR-1269 during HCC progression has not been unfolded. [score:2]
We have shown that miR-1269 functions in regulating cell growth, tumorigenicity, and cell cycle progression. [score:2]
miR-1269 Hepatocellular cancer Proliferation FOXO1 Hepatocellular carcinoma (HCC) is one of the most common cancers in the world, and the third most common cause of cancer-related death, especially in Asian countries [1, 2]. [score:1]
B. Real-time PCR analysis of miR-1269 and western blotting analysis of FOXO1 in 8 paired cancerous tissues (T) and their adjacent noncancerous hepatic tissues (N). [score:1]
A. Sequence alignment of miR-1269, miR-1269 mutant (miR-1269-mut), and putative FOXO1-3’UTR. [score:1]
In conclusion, this study revealed that miR-1269 might have potential function to determine human intestinal epithelial cell fate. [score:1]
The aim of the current study was to elucidate the role of miR-1269 in the pathogenesis of HCC. [score:1]
The stably engineered pMSCV-miR-1269 cell line was established using standard methods [14]. [score:1]
Herein, for the first time we have revealed an important link between miR-1269 and HCC progression. [score:1]
A region of the human FOXO1 3’-UTR containing three miR-1269 binding sites was amplified by PCR and cloned into vector pGL3 (Promega, Madison, WI, USA). [score:1]
E. The effect of miR-1269 on cell cycle progression of the indicated cell lines analyzed by flow cytometry. [score:1]
Given that our results indicated miR-1269 could influence HCC cell proliferation, we investigated its effects on the expression level of FOXO1 downstream genes, such as p21 [Cip1], cyclin D1, and Rb. [score:1]
As shown in Figure  4A, there are three miR-1269 binding sites in the FOXO1 mRNA 3’UTR, including one conserved and two poorly conserved binding sites. [score:1]
Dalmasso, et al. found that transfection of enterocyte-like Caco2-BBE cells with antisense of mature miR-1269 could decrease growth rate and trans-epithelial resistance of the cells, indicating their shift toward colonocyte-like HT29-Cl cells, which is one clone of human colonic cancer HT29 cells [29]. [score:1]
Briefly, pMSCV-miR-1269 was cotransfected with the packaging plasmid into 293FT cells. [score:1]
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[+] score: 7
Some of the largest differences were observed for MIR767 and MIR1269, both absent in the hTERT-HPNE cells but highly expressed in the cancer derived PANC-1 cells. [score:3]
Differential miRNA expression levels included higher levels of MIR767, MIR135B, MIR1269, MIR182, MIR183, and MIR203 and lower levels of MIR494, MIR424, MIR381, MIR452, and MIR155 in PANC-1 cells. [score:3]
The function of MIR767 and MIR1269 is largely unknown although the latter may be important during differentiation of human embryonic stem cells [42]. [score:1]
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[+] score: 6
Overexpression of miR-1269 accelerates cell proliferation in HCC aiding in directly suppressing FOXO1 (MAPK/ERK) signaling [30]. [score:6]
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[+] score: 2
Other miRNAs from this paper: hsa-mir-18a, hsa-mir-21, hsa-mir-122, hsa-mir-3928
In addition, a previous study from our laboratory showed that miR-1269b is induced by HBx in an NF-κB -dependent manner, thereby up -regulating CDC40 to promote HCC cell proliferation and migration [12]. [score:2]
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[+] score: 1
The hsa-miR-1269b and hsa-miR-1034-3p miRNAs had the largest percentage (100%) of edited bases in the NC group. [score:1]
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[+] score: 1
01 Down 4.40E-07 hsa-miR-4488 5.95 Up 4.10E-35 hsa-miR-1269b −6.74 Down 3.15E-06 hsa-miR-296-5p 5.84 Up 3.88E-78 hsa-miR-3674 −6.74 Down 3.16E-06 hsa-miR-4454 5.19 Up 3.07E-85 hsa-miR-3910 −6.74 Down 3.17E-06 hsa-miR-4687-3p 4.37 Up 8.32E-26 hsa-miR-642a-3p −6.74 Down 5.10E-32 hsa-miR-3654 3.38 Up 1.21E-25 hsa-miR-486-5p −6.46 Down 2.81E-100 hsa-miR-577 2.94 Up 8.64E-05 hsa-miR-203 −6.30 Down 3.19E-89 hsa-miR-4508 2.9 Up 5.94E-06 hsa-miR-1277-3p −6.16 Down 3.01E-41 hsa-miR-3687 2.49 Up 2.04E-05 hsa-miR-1277-5p −5. [score:1]
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