Long non-coding RNA AC023115.3 suppresses chemoresistance of glioblastoma by reducing autophagy

Publication date: August 2017
Source:Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, Volume 1864, Issue 8
Author(s): Binbin Ma, Zhongbo Yuan, Li Zhang, Peng Lv, Ting Yang, Jinxia Gao, Ning Pan, Qiong Wu, Jiacheng Lou, Chuanchun Han, Bo Zhang
Malignant glioma is an aggressive brain cancer that responds poorly to chemotherapy. However, the molecular mechanism underlying the development of chemoresistance in glioma is not well-understood. In this study, we show that long non-coding RNA AC023115.3 is induced by cisplatin in human glioblastoma cells and that elevated AC023115.3 promotes cisplatin-induced apoptosis by inhibiting autophagy. Further mechanistic studies revealed that AC023115.3 acts as a competing endogenous RNA for miR-26a and attenuates the inhibitory effect of miR-26a on GSK3β, a proline-directed serine-threonine kinase that promotes the degradation of Mcl1, leading to an increase in GSK3β and a decrease in autophagy. Additionally, we discovered that AC023115.3 improves chemosensitivity of glioma cells to cisplatin by regulating the miR-26a-GSK3β-Mcl1 pathway. Thus, these data indicate that the AC023115.3-miR-26a-GSK3β signalling axis plays an important role in reducing the chemoresistance of glioma.



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