Homepage    |    About Us    |    News and Events    |    Archive    |    Search    |    Submission    |    Links    |    Contact    |    Dilute urine for drug test    |   �������İ�
��
��
Aim and Scope
Editorial Policies
Editorial Board
Guide for Authors
Submit a Manuscript
News and Events
Guide for Reviewers
Review a Manuscript
Editorial Office
Customer Services
FAQ
��
Abstract
��

Vol41 No.5: 341-351

 

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)

 

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.

 

Received: 2008-11-1����Accepted: 2009-2-25

 

*Corresponding author . Tel: +86-512-65880119; Fax: +86-512-65190599; E-mail: [email protected]

 

Browse:349

��
��
Copyright 1999-2010    Acta Biochimica et Biophysica Sinica    All Rights Reserved

Address: Room 407, Building 31B, 319 Yueyang Road, Shanghai, 200031 P.R. China
Fax: 86-21-54920954    Email: [email protected] & [email protected]

��