MiR-16-1 Targeted Silences Far Upstream Element Binding Protein 1 to Advance the Chemosensitivity to Adriamycin in Gastric Cancer

Pathology oncology research: POR

Danyi Zhao¹ 

[1]Dalian Medical University

关键词: Gastric cancer;    microRNA-16-1;    Far upstream element binding protein 1;    Chemosensitivity;    Adriamycin;   

DOI  :  10.1007/s12253-017-0263-x

学科分类：生理学与病理学

来源: Springer

【 摘 要 】

Chemotherapy can prevent metastasis and recurrence of gastric cancer (GC), and is a well supplement for operation. But, chemotherapy resistance has severely restricted the application of chemotherapy. This study aimed to investigate the regulatory roles and molecular mechanism of miR-16-1 to the chemosensitivity to adriamycin in GC. In this study, the expression of miR-16-1 and FUBP1 was down-regulated and up-regulated respectively in adriamycin-resistant GC tissues and cell lines, and represented a negative relationship between them. MiR-16-1 could silence FUBP1 directly and specifically, FUBP1 was a target gene of miR-16-1. Silence of FUBP1 inhibited the half maximal inhibitory concentration (IC50) of SGC7901/AR cell line to adriamycin, chemosensitivity enhanced significantly. Moreover, FUBP1 silence in SGC7901/AR cell line also inhibited proliferation and invasion, and advanced cell apoptosis. To sum up, the expression of miR-16-1 was positively related with the chemosensitivity of GC to adriamycin, and miR-16-1 could targeted silence FUBP1 to advance the chemosensitivity to adriamycin in GC, which might be a novel potential therapeutic target for GC.

【 授权许可】

CC BY