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Deciphering the Role of Autophagy in Treatment of Resistance Mechanisms in Glioblastoma

Authors
 Imran Khan  ;  Mohammad Hassan Baig  ;  Sadaf Mahfooz  ;  Moniba Rahim  ;  Busra Karacam  ;  Elif Burce Elbasan  ;  Ilya Ulasov  ;  Jae-June Dong  ;  Mustafa Aziz Hatiboglu 
Citation
 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, Vol.22(3) : 1318, 2021-01 
Journal Title
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
ISSN
 1661-6596 
Issue Date
2021-01
Keywords
autophagy ; chemoresistance ; glioblastoma ; glioma stem cells ; molecular targets ; radioresistance
Abstract
Autophagy is a process essential for cellular energy consumption, survival, and defense mechanisms. The role of autophagy in several types of human cancers has been explicitly explained; however, the underlying molecular mechanism of autophagy in glioblastoma remains ambiguous. Autophagy is thought to be a "double-edged sword", and its effect on tumorigenesis varies with cell type. On the other hand, autophagy may play a significant role in the resistance mechanisms against various therapies. Therefore, it is of the utmost importance to gain insight into the molecular mechanisms deriving the autophagy-mediated therapeutic resistance and designing improved treatment strategies for glioblastoma. In this review, we discuss autophagy mechanisms, specifically its pro-survival and growth-suppressing mechanisms in glioblastomas. In addition, we try to shed some light on the autophagy-mediated activation of the cellular mechanisms supporting radioresistance and chemoresistance in glioblastoma. This review also highlights autophagy's involvement in glioma stem cell behavior, underlining its role as a potential molecular target for therapeutic interventions.
Files in This Item:
T202100442.pdf Download
DOI
10.3390/ijms22031318
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Family Medicine (가정의학교실) > 1. Journal Papers
Yonsei Authors
Dong, Jae June(동재준) ORCID logo https://orcid.org/0000-0002-2420-2155
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/182111
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