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MicroRNA-1 (miR-1) inhibits gastric cancer cell proliferation and migration by targeting MET.

Han C, Zhou Y, An Q, Li F, Li D, Zhang X, Yu Z, Zheng L, Duan Z, Kan Q - Tumour Biol. (2015)

Bottom Line: MicroRNAs (miRs) are short endogenous non-coding RNAs that act as posttranscriptional regulatory factors of gene expression.Cell protein expression of the miR-1 target gene MET was analyzed by Western blotting.MET siRNA also inhibited proliferation and migration in both cell lines.

View Article: PubMed Central - PubMed

Affiliation: Department of Clinical Pharmacology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, People's Republic of China.

ABSTRACT
MicroRNAs (miRs) are short endogenous non-coding RNAs that act as posttranscriptional regulatory factors of gene expression. Downregulation of miR-1 has been reported in gastric cancer; however, the mechanisms underlying its functions via target genes in gastric cancer remain largely unknown. The purpose of this study was to investigate the mechanism by which miR-1 inhibits gastric cancer cell proliferation and migration. The effects of miR-1 on gastric cancer cell proliferation and migration were determined by MTT and wound-healing assays. Cell protein expression of the miR-1 target gene MET was analyzed by Western blotting. Finally, MET expression was evaluated by immunohistochemistry in a stomach tumor tissue microarray (TMA). Ectopic expression of miR-1 inhibited proliferation and migration in both AGS and SGC-7901 gastric cancer cell lines. miR-1 directly targets the MET gene and downregulates its expression. MET siRNA also inhibited proliferation and migration in both cell lines. Immunohistochemistry revealed significantly higher MET expression levels in gastric cancer tissues compared with matched adjacent non-cancer tissues. These findings indicate that the miR-1/MET pathway is a potential therapeutic target due to its crucial role in gastric cancer cell proliferation and migration.

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MET protein expression in miR-1 transfectants. a MiR-1 and non-specific miR mimics were transfected into AGS cells, respectively. MET and survivin protein expression levels were determined after 72 h. b, c Quantification of protein expression using the Odyssey Infrared Imaging System and the application software. The data indicate that MET and survivin protein expression levels were suppressed by 68 and 71.9 %, respectively. d, e, f MET and survivin protein expression in SGC-7901 cells. Both proteins were downregulated by 64.6 and 41.6 %, respectively
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Fig3: MET protein expression in miR-1 transfectants. a MiR-1 and non-specific miR mimics were transfected into AGS cells, respectively. MET and survivin protein expression levels were determined after 72 h. b, c Quantification of protein expression using the Odyssey Infrared Imaging System and the application software. The data indicate that MET and survivin protein expression levels were suppressed by 68 and 71.9 %, respectively. d, e, f MET and survivin protein expression in SGC-7901 cells. Both proteins were downregulated by 64.6 and 41.6 %, respectively

Mentions: To assess the mechanism by which miR-1 inhibits gastric cancer cell growth, miR-1 mimics (40 nmol/L) were introduced into proliferating AGS and SGC-7901 cells. As shown in Fig. 3, MET protein expression was significantly downregulated in miR-1 transfectants in comparison with the control cells. These results indicated that MET is a common target gene for miR-1. In AGS and SGC-7901, the expression levels of MET were downregulated to 32 and 35.4 %, respectively.Fig. 3


MicroRNA-1 (miR-1) inhibits gastric cancer cell proliferation and migration by targeting MET.

Han C, Zhou Y, An Q, Li F, Li D, Zhang X, Yu Z, Zheng L, Duan Z, Kan Q - Tumour Biol. (2015)

MET protein expression in miR-1 transfectants. a MiR-1 and non-specific miR mimics were transfected into AGS cells, respectively. MET and survivin protein expression levels were determined after 72 h. b, c Quantification of protein expression using the Odyssey Infrared Imaging System and the application software. The data indicate that MET and survivin protein expression levels were suppressed by 68 and 71.9 %, respectively. d, e, f MET and survivin protein expression in SGC-7901 cells. Both proteins were downregulated by 64.6 and 41.6 %, respectively
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4644207&req=5

Fig3: MET protein expression in miR-1 transfectants. a MiR-1 and non-specific miR mimics were transfected into AGS cells, respectively. MET and survivin protein expression levels were determined after 72 h. b, c Quantification of protein expression using the Odyssey Infrared Imaging System and the application software. The data indicate that MET and survivin protein expression levels were suppressed by 68 and 71.9 %, respectively. d, e, f MET and survivin protein expression in SGC-7901 cells. Both proteins were downregulated by 64.6 and 41.6 %, respectively
Mentions: To assess the mechanism by which miR-1 inhibits gastric cancer cell growth, miR-1 mimics (40 nmol/L) were introduced into proliferating AGS and SGC-7901 cells. As shown in Fig. 3, MET protein expression was significantly downregulated in miR-1 transfectants in comparison with the control cells. These results indicated that MET is a common target gene for miR-1. In AGS and SGC-7901, the expression levels of MET were downregulated to 32 and 35.4 %, respectively.Fig. 3

Bottom Line: MicroRNAs (miRs) are short endogenous non-coding RNAs that act as posttranscriptional regulatory factors of gene expression.Cell protein expression of the miR-1 target gene MET was analyzed by Western blotting.MET siRNA also inhibited proliferation and migration in both cell lines.

View Article: PubMed Central - PubMed

Affiliation: Department of Clinical Pharmacology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, People's Republic of China.

ABSTRACT
MicroRNAs (miRs) are short endogenous non-coding RNAs that act as posttranscriptional regulatory factors of gene expression. Downregulation of miR-1 has been reported in gastric cancer; however, the mechanisms underlying its functions via target genes in gastric cancer remain largely unknown. The purpose of this study was to investigate the mechanism by which miR-1 inhibits gastric cancer cell proliferation and migration. The effects of miR-1 on gastric cancer cell proliferation and migration were determined by MTT and wound-healing assays. Cell protein expression of the miR-1 target gene MET was analyzed by Western blotting. Finally, MET expression was evaluated by immunohistochemistry in a stomach tumor tissue microarray (TMA). Ectopic expression of miR-1 inhibited proliferation and migration in both AGS and SGC-7901 gastric cancer cell lines. miR-1 directly targets the MET gene and downregulates its expression. MET siRNA also inhibited proliferation and migration in both cell lines. Immunohistochemistry revealed significantly higher MET expression levels in gastric cancer tissues compared with matched adjacent non-cancer tissues. These findings indicate that the miR-1/MET pathway is a potential therapeutic target due to its crucial role in gastric cancer cell proliferation and migration.

Show MeSH
Related in: MedlinePlus