Journal
APOPTOSIS
Volume 23, Issue 11-12, Pages 563-575Publisher
SPRINGER
DOI: 10.1007/s10495-018-1480-9
Keywords
Autophagy; Cell death; Chemoresistance; Glioblastoma; Radioresistance
Categories
Funding
- Soy Health Research Program (SHRP, United Soybean Board, Chesterfield, MO, USA)
- South Carolina Spinal Cord Injury Research Fund (Columbia, SC, USA) [SCIRF-2015-I-01]
- National Institutes of Health (Bethesda, MD, USA) [CA-091460, NS-057811]
- NATIONAL CANCER INSTITUTE [R01CA091460] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS057811] Funding Source: NIH RePORTER
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Autophagy is an evolutionarily conserved catabolic process that plays an essential role in maintaining cellular homeostasis by degrading unneeded cell components. When exposed to hostile environments, such as hypoxia or nutrient starvation, cells hyperactivate autophagy in an effort to maintain their longevity. In densely packed solid tumors, such as glioblastoma, autophagy has been found to run rampant due to a lack of oxygen and nutrients. In recent years, targeting autophagy as a way to strengthen current glioblastoma treatment has shown promising results. However, that protective autophagy inhibition or autophagy overactivation is more beneficial, is still being debated. Protective autophagy inhibition would lower a cell's previously activated defense mechanism, thereby increasing its sensitivity to treatment. Autophagy overactivation would cause cell death through lysosomal overactivation, thus introducing another cell death pathway in addition to apoptosis. Both methods have been proven effective in the treatment of solid tumors. This systematic review article highlights scenarios where both autophagy inhibition and activation have proven effective in combating chemoresistance and radioresistance in glioblastoma, and how autophagy may be best utilized for glioblastoma therapy in clinical settings.
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