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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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Transfection with miR-1 inhibits gastric cancer AGS and SGC-7901 cell growth. a, b To verify the expression levels of miR-1 in these two gastric cancer cell lines after transfecting miR-1 mimics for 48 h. c, d AGS and SGC-7901 cells were transfected with miR-1 mimics and non-specific miR mimics at 5–80 nM, respectively, and incubated for up to 72 h in a medium containing 10 % FBS. Cell growth was measured by MTT-based cell proliferation assay. The experiment was performed in triplicate
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Fig1: Transfection with miR-1 inhibits gastric cancer AGS and SGC-7901 cell growth. a, b To verify the expression levels of miR-1 in these two gastric cancer cell lines after transfecting miR-1 mimics for 48 h. c, d AGS and SGC-7901 cells were transfected with miR-1 mimics and non-specific miR mimics at 5–80 nM, respectively, and incubated for up to 72 h in a medium containing 10 % FBS. Cell growth was measured by MTT-based cell proliferation assay. The experiment was performed in triplicate

Mentions: To understand the potential function of miR-1 in gastric cancer, MTT assay was carried out to assess the proliferation of gastric cancer cells after transfection with miR-1 mimics. As shown in Fig. 1a, b, the expression levels of miR-1 were upregulated in these two gastric cancer cell lines as confirmed by SYBR Green real-time RT-PCR. Then we performed MTT to determine the function of miR-1. The results showed that the two gastric cancer cell lines were significantly inhibited in miR-1 transfectants in comparison with cells transfected with the non-specific miR negative control (Fig. 1c, d). These results indicated that overexpression of miR-1 inhibited proliferation of gastric cancer cells in a dose-dependent manner in vitro (Fig. 1). Furthermore, wound-healing assay data showed significantly different widths for the residual gaps obtained in the miR-1 transfection and non-specific miR control groups, especially at 72 h (Fig. 2, P < 0.001). This experiment was repeated for three times.Fig. 1


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)

Transfection with miR-1 inhibits gastric cancer AGS and SGC-7901 cell growth. a, b To verify the expression levels of miR-1 in these two gastric cancer cell lines after transfecting miR-1 mimics for 48 h. c, d AGS and SGC-7901 cells were transfected with miR-1 mimics and non-specific miR mimics at 5–80 nM, respectively, and incubated for up to 72 h in a medium containing 10 % FBS. Cell growth was measured by MTT-based cell proliferation assay. The experiment was performed in triplicate
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

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

Fig1: Transfection with miR-1 inhibits gastric cancer AGS and SGC-7901 cell growth. a, b To verify the expression levels of miR-1 in these two gastric cancer cell lines after transfecting miR-1 mimics for 48 h. c, d AGS and SGC-7901 cells were transfected with miR-1 mimics and non-specific miR mimics at 5–80 nM, respectively, and incubated for up to 72 h in a medium containing 10 % FBS. Cell growth was measured by MTT-based cell proliferation assay. The experiment was performed in triplicate
Mentions: To understand the potential function of miR-1 in gastric cancer, MTT assay was carried out to assess the proliferation of gastric cancer cells after transfection with miR-1 mimics. As shown in Fig. 1a, b, the expression levels of miR-1 were upregulated in these two gastric cancer cell lines as confirmed by SYBR Green real-time RT-PCR. Then we performed MTT to determine the function of miR-1. The results showed that the two gastric cancer cell lines were significantly inhibited in miR-1 transfectants in comparison with cells transfected with the non-specific miR negative control (Fig. 1c, d). These results indicated that overexpression of miR-1 inhibited proliferation of gastric cancer cells in a dose-dependent manner in vitro (Fig. 1). Furthermore, wound-healing assay data showed significantly different widths for the residual gaps obtained in the miR-1 transfection and non-specific miR control groups, especially at 72 h (Fig. 2, P < 0.001). This experiment was repeated for three times.Fig. 1

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