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MicroRNA‑218 enhances gastric cancer cell cisplatin sensitivity by targeting survivin
Author(s) -
Zhandong Zhang,
Ye Kong,
Wei Yang,
Bin Zhang,
Fei Ma,
Hongxing Liu,
Yawei Hua
Publication year - 2018
Publication title -
experimental and therapeutic medicine
Language(s) - English
Resource type - Journals
eISSN - 1792-1015
pISSN - 1792-0981
DOI - 10.3892/etm.2018.6802
Subject(s) - survivin , cisplatin , microrna , downregulation and upregulation , oncogene , cancer research , apoptosis , mtt assay , cell cycle , cell , cancer , cell growth , cancer cell , biology , microbiology and biotechnology , chemistry , chemotherapy , biochemistry , gene , genetics
Gastric cancer (GC) is one of the most prevalent types of cancer worldwide. Cisplatin based chemotherapy is the primary strategy implemented for the treatment of G; however, chemoresistance is a major problem. Previous studies have indicated that microRNAs (miRs) are associated with chemoresistance in various types of cancer and that miR-218 specifically, serves important roles in the growth of GC cells. The present study assessed the potential biological roles of miR-218 in GC cell cisplatin (DDP) resistance. The results obtained from a polymerase chain reaction assay indicated that the expression of miR-218 was decreased in cisplatin resistant SGC7901/DDP cells compared with SGC7901 cells. Furthermore, MTT results indicated that the upregulation of miR-218 expression significantly enhanced SGC7901/DDP cell sensitivity to DDP. The results of a dual-luciferase assay indicated that survivin was a direct target gene of miR-218. Results also demonstrated that miR-218 was overexpressed in SGC7901/DDP cells and that the downregulation of survivin expression enhanced SGC7901/DDP cell sensitivity to DDP. Further study demonstrated that the upregulation of miR-218 decreased the expression of survivin in SGC7901/DDP cells and induced apoptosis. The findings of the present study indicated that the induction of miR-218 enhanced GC cell DDP resistance via the regulation of survivin, which may potentially benefit the clinical treatment of GC in the future.

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