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Acta Biochimica et Biophysica Sinica Advance Access originally published online on April 3, 2009
Acta Biochimica et Biophysica Sinica 2009 41(5):341-351; doi:10.1093/abbs/gmp028
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© The Author 2009. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.

The role of autophagy in sensitizing malignant glioma cells to radiation therapy

Wenzhuo Zhuang1, Zhenghong Qin2 and Zhongqin Liang1,2,*

1 Department of Pharmacology, Soochow University School of Medicine, Suzhou 215123, China
2 Laboratory of Aging and Nervous Diseases, Soochow University School of Medicine, Suzhou 215123, China

* Correspondence address. Tel: +86-512-65880119; Fax: +86-512-65190599; E-mail: lzq2003cn{at}yahoo.com.cn


  Abstract

Malignant gliomas represent the majority of primary brain tumors. The current standard treatments for malignant gliomas include surgical resection, radiation therapy, and chemotherapy. Radiotherapy, a standard adjuvant therapy, confers some survival advantages, but resistance of the glioma cells to the efficacy of radiation limits the success of the treatment. The mechanisms underlying glioma cell radioresistance have remained elusive. Autophagy is a protein degradation system characterized by a prominent formation of double-membrane vesicles in the cytoplasm. Recent studies suggest that autophagy may be important in the regulation of cancer development and progression and in determining the response of tumor cells to anticancer therapy. Also, autophagy is a novel response of glioma cells to ionizing radiation. Autophagic cell death is considered programmed cell death type II, whereas apoptosis is programmed cell death type I. These two types of cell death are predominantly distinctive, but many studies demonstrate a cross-talk between them. Whether autophagy in cancer cells causes death or protects cells is controversial. The regulatory pathways of autophagy share several molecules. PI3K/Akt/mTOR, DNA-PK, tumor suppressor genes, mitochondrial damage, and lysosome may play important roles in radiation-induced autophagy in glioma cells. Recently, a highly tumorigenic glioma tumor subpopulation, termed cancer stem cell or tumor-initiating cell, has been shown to promote therapeutic resistance. This review summarizes the main mediators associated with radiation-induced autophagy in malignant glioma cells and discusses the implications of the cancer stem cell hypothesis for the development of future therapies for brain tumors.

Keywords    autophagy; glioma cell; radiation; PI3K/Akt/mTOR; DNA-PK

Received: November 1, 2008; Accepted: February 25, 2008
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