Role of autophagy in therapeutic resistance of glioblastoma

Chia Hung Chien, Wei Ting Hsueh, Jian Ying Chuang, Kwang Yu Chang

Research output: Contribution to journalReview articlepeer-review

10 Citations (Scopus)


Patients with glioblastoma (GBM), a malignant brain tumor, exhibit a mean survival of less than 1.5 years. Despite treatment, the disease eventually develops resistance, resulting in disease relapse. Autophagy is a process of degradation and clearance that is activated to maintain cellular homeostasis. Its roles in cancer disease course and the treatment response, however, are controversial. In GBM, accumulating evidence has indicated that autophagy can protect cells, especially those with stemness features, causing the development of cell resistance. In this review, we discuss the impact of the cell reaction to currently active treatments, including temozolomide, radiation, tumor treating fields, bevacizumab (Avastin), etoposide (VP-16), cisplatin (CDDP), and carmustine (BCNU). Most of these induce the up-regulation of autophagy through signaling pathways of DNA damage response, reactive oxygen species, hypoxia, retinoblastoma, AMP-activated protein kinase, AKT/mTOR and MST4 kinase affecting cell fate by altering cell metabolism, cell death, and DNA repair. Treatment-related autophagy may be modulated by combining autophagy inhibitors such as chloroquine or antioxidants to prevent the development of resistance, thus improving cancer treatment.

Original languageEnglish
Article number66
JournalJournal of Cancer Metastasis and Treatment
Publication statusPublished - 2019

All Science Journal Classification (ASJC) codes

  • Oncology


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