Open AccessMiR‐634 sensitizes glioma cells to temozolomide by targeting CYR 61 through Raf‐ ERK signaling pathway
Author(s) -
Tan Zhigang,
Zhao Jizong,
Jiang Yugang
Publication year - 2018
Publication title -
cancer medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 53
ISSN - 2045-7634
DOI - 10.1002/cam4.1351
Subject(s) - temozolomide , glioma , medicine , cancer research , mapk/erk pathway , microrna , signal transduction , biology , gene , microbiology and biotechnology , biochemistry
Glioma is the most common intracranial malignant tumors, accounting for about 40% of intracranial tumors. Primary or secondary drug resistance is one of the main reasons for the failure of treatment. The oncogenic or tumor‐suppressive roles of miR‐634 have been revealed in different types of cancer. However, the role of miR‐634 in glioma remains unknown and whether miR‐634 could sensitize glioma cells to temozolomide also is unclear. Here, we aim to investigate the biological function of miR‐634 and the possible mechanisms in glioma. In this study, we found that miR‐634 was downregulated in glioma tissues compared with normal brain tissues, and its expression was associated with tumor size and WHO grade. Importantly, glioma patients with low miR‐634 expression showed a shorter survival time than patients which had high expression of miR‐634. This study also showed that miR‐634 was decreased in temozolomide‐resistant glioma cells, and restoration of miR‐634 could sensitize the resistant cells to temozolomide by targeting CYR 61 through Raf‐ ERK signaling. Our study provides a potential target for overcome drug resistance in glioma.