Journal
BIOMEDICINES
Volume 10, Issue 6, Pages -Publisher
MDPI
DOI: 10.3390/biomedicines10061308
Keywords
glioblastoma; chemoresistance; cancer stem cells; temozolomide
Categories
Funding
- National Research Foundation of Korea (NRF) - Korea government (MSIT) [NRF-2020R1A2C2005793]
- National Research Foundation of Korea (NRF) - Ministry of Science and ICT [2020M2D9A2094156]
- BK21 FOUR Program by Pusan National University Research Grant, 2021-2022
- National Research Foundation of Korea [2020M2D9A2094156] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Glioblastoma (GBM) is a highly malignant brain tumor that is resistant to current therapies. This review focuses on the resistance mechanisms of GBM, particularly towards temozolomide (TMZ), and summarizes the recent findings on the intrinsic and extrinsic mechanisms of chemoresistance in GBM stem cells (GSCs). It also discusses novel therapeutic strategies, such as molecular targeting, autophagy inhibition, oncolytic viral therapy, drug repositioning, and targeting of GSC niches, to eliminate GSCs and improve GBM therapy.
Glioblastoma (GBM) is the most malignant primary brain tumor. The current standard approach in GBM is surgery, followed by treatment with radiation and temozolomide (TMZ); however, GBM is highly resistant to current therapies, and the standard of care has not been revised over the last two decades, indicating an unmet need for new therapies. GBM stem cells (GSCs) are a major cause of chemoresistance due to their ability to confer heterogeneity and tumorigenic capacity. To improve patient outcomes and survival, it is necessary to understand the properties and mechanisms underlying GSC chemoresistance. In this review, we describe the current knowledge on various resistance mechanisms of GBM to therapeutic agents, with a special focus on TMZ, and summarize the recent findings on the intrinsic and extrinsic mechanisms of chemoresistance in GSCs. We also discuss novel therapeutic strategies, including molecular targeting, autophagy inhibition, oncolytic viral therapy, drug repositioning, and targeting of GSC niches, to eliminate GSCs, from basic research findings to ongoing clinical trials. Although the development of effective therapies for GBM is still challenging, this review provides a better understanding of GSCs and offers future directions for successful GBM therapy.
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