Oncotarget

Research Papers:

miR-29c contribute to glioma cells temozolomide sensitivity by targeting O6-methylguanine-DNA methyltransferases indirectly

Songhua Xiao, Zhen Yang, Xingsheng Qiu, Ruiyan Lv, Jun Liu, Ming Wu, Yiwei Liao and Qing Liu _

PDF  |  HTML  |  How to cite  |  Order a Reprint

Oncotarget. 2016; 7:50229-50238. https://doi.org/10.18632/oncotarget.10357

Metrics: PDF 2256 views  |   HTML 1982 views  |   ?  


Abstract

Songhua Xiao1,*, Zhen Yang2,*, Xingsheng Qiu3,*, Ruiyan Lv1, Jun Liu1, Ming Wu4, Yiwei Liao4, Qing Liu4

1Department of Neurology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guanzhou, Guangdong, China

2Department of Hypertension and Vascular Disease, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, Guangdong, China

3Department of Radiation Oncology, Sun Yat-Sen Memorial Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China

4Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan, China

*These authors have contributed equally to this work

Correspondence to:

Qing Liu, email: chingliucn@yahoo.com

Keywords: glioblastoma, TMZ, MGMT, miR-29c, chemoresistance

Received: November 28, 2015    Accepted: May 28, 2016    Published: July 1, 2016

ABSTRACT

Temozolomide (TMZ) is the most commonly used alkylating agent in glioma chemotherapy. However growing resistance to TMZ remains a major challenge to clinicians. The DNA repair protein O6-methylguanine-DNA methytransferase (MGMT) plays critical roles in TMZ resistance. Promoter methylation can inhibit MGMT expression and increase chemosensitivity. Here, we described a novel mechanism regulating MGMT expression. We showed that miR-29c suppressed MGMT expression indirectly via targeting specificity protein 1 (Sp1). MiR-29c overexpression increased TMZ efficacy in cultured glioma cells and in mouse xenograft models. The miR-29c levels were positively correlated with patient outcomes. Our data suggest miR-29c may be potential therapeutic targets for glioma treatment.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.
PII: 10357