Open AccessLong noncoding RNA MALAT 1 knockdown reverses chemoresistance to temozolomide via promoting micro RNA ‐101 in glioblastoma
Author(s) -
Cai Tao,
Liu Yu,
Xiao Jie
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/cam4.1384
Subject(s) - malat1 , temozolomide , gene knockdown , cancer research , long non coding rna , downregulation and upregulation , apoptosis , u87 , microrna , chemotherapy , cell growth , biology , glioblastoma , gene , genetics
Glioblastoma ( GBM ) is the most common and lethal tumor of the central nervous system with highly infiltrative and resistant to chemotherapy. Temozolomide ( TMZ ) is widely used as the first‐line treatment for the therapy of GBM . However, a considerable percentage inherent or acquired resistance in GBM accounts for many treatment failures of the TMZ chemotherapy. Therefore, a deeper understanding of the molecular characteristics underlying TMZ resistance and the identification of novel therapeutic target is urgent. Here, we show that MALAT 1 was significantly upregulated in TMZ ‐resistant GBM cells. On the other hand, MALAT 1 knockdown reduces TMZ resistance of GBM cells both in vitro and in vivo by inhibiting cell proliferation and promoting apoptosis. We also show that miR‐101 overexpression reduced TMZ resistance of GBM cells and played an antagonistic role compared with MALAT 1. Importantly, we demonstrate that MALAT 1 promoted the chemoresistance through suppressing miR‐101 signaling pathway via directly binding it in GBM cells. In conclusion, our study indicates that knockdown of MALAT 1 reverses chemoresistance to TMZ via promoting miR‐101 regulatory network in GBM and thus offers a novel prognostic marker and potential target for GBM TMZ ‐based chemotherapy.