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DOI 10.1016/j.clinre.2016.05.006

Медицинская библиотека · Clinics and research in hepatology and gastroenterology · 2016

MicroRNA-214 promotes peritoneal metastasis through regulating PTEN negatively in gastric cancer.

Xin Ruijuan, Bai Feihu, Feng Yaning, Jiu Mengna, Liu Xiaogang, Bai Fangyun, Nie Yongzhan, Fan Daiming

СтатьяПеревод пока не подготовлен

Аннотация

BACKGROUND AND

OBJECTIVE

We aimed to investigate the effects of microRNA-214 (miR-214) on peritoneal metastasis as well as to elucidate its regulatory mechanism in gastric cancer (GC).

METHODS

The expression levels of miR-214 in human GC cell lines MKN-28NM, MKN-28M, GC9811 and GC9811-P were analyzed by quantitative real-time PCR. Lentiviral miR-214, lentiviral miR-214 inhibitor, and empty lentiviral vector were transfected to GC cell lines, respectively. The roles of miR-214 in cell invasion, migration, proliferation and colony-forming ability were then analyzed. Besides, the expression levels of PTEN in different transfected cells were determined by western blot analysis.

RESULTS

We found that miR-214 was up-regulated in GC9811-P cells with high metastatic potential to the peritoneum compared with that in GC9811 cells. In addition, in vitro overexpression of miR-214 promoted cell invasion, migration, proliferation and colony-forming ability of GC9811 cells, while down-regulation of miR-214 had opposite effects in GC9811-P cells. Besides, overexpression of miR-214 in GC9811 cells markedly down-regulated PTEN expression, whereas down-regulation of miR-214 in GC9811-P cells significantly increased PTEN expression.

CONCLUSIONS

Our findings indicate that miR-214 may promote peritoneal metastasis of GC cells via down-regulation of PTEN, thus leading to the progression of GC.

Для цитирования: Xin Ruijuan, Bai Feihu, Feng Yaning, Jiu Mengna, Liu Xiaogang, Bai Fangyun, Nie Yongzhan, Fan Daiming. MicroRNA-214 promotes peritoneal metastasis through regulating PTEN negatively in gastric cancer.. Clinics and research in hepatology and gastroenterology. 2016. DOI: 10.1016/j.clinre.2016.05.006.

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