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Friend or Foe: Paradoxical Roles of Autophagy in Gliomagenesis

Glioblastoma multiforme (GBM) is the most common and aggressive type of primary brain tumor in adults, with a poor median survival of approximately 15 months after diagnosis. Despite several decades of intensive research on its cancer biology, treatment for GBM remains a challenge. Autophagy, a fund...

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Autores principales: Batara, Don Carlo Ramos, Choi, Moon-Chang, Shin, Hyeon-Uk, Kim, Hyunggee, Kim, Sung-Hak
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8227518/
https://www.ncbi.nlm.nih.gov/pubmed/34204169
http://dx.doi.org/10.3390/cells10061411
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author Batara, Don Carlo Ramos
Choi, Moon-Chang
Shin, Hyeon-Uk
Kim, Hyunggee
Kim, Sung-Hak
author_facet Batara, Don Carlo Ramos
Choi, Moon-Chang
Shin, Hyeon-Uk
Kim, Hyunggee
Kim, Sung-Hak
author_sort Batara, Don Carlo Ramos
collection PubMed
description Glioblastoma multiforme (GBM) is the most common and aggressive type of primary brain tumor in adults, with a poor median survival of approximately 15 months after diagnosis. Despite several decades of intensive research on its cancer biology, treatment for GBM remains a challenge. Autophagy, a fundamental homeostatic mechanism, is responsible for degrading and recycling damaged or defective cellular components. It plays a paradoxical role in GBM by either promoting or suppressing tumor growth depending on the cellular context. A thorough understanding of autophagy’s pleiotropic roles is needed to develop potential therapeutic strategies for GBM. In this paper, we discussed molecular mechanisms and biphasic functions of autophagy in gliomagenesis. We also provided a summary of treatments for GBM, emphasizing the importance of autophagy as a promising molecular target for treating GBM.
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spelling pubmed-82275182021-06-26 Friend or Foe: Paradoxical Roles of Autophagy in Gliomagenesis Batara, Don Carlo Ramos Choi, Moon-Chang Shin, Hyeon-Uk Kim, Hyunggee Kim, Sung-Hak Cells Review Glioblastoma multiforme (GBM) is the most common and aggressive type of primary brain tumor in adults, with a poor median survival of approximately 15 months after diagnosis. Despite several decades of intensive research on its cancer biology, treatment for GBM remains a challenge. Autophagy, a fundamental homeostatic mechanism, is responsible for degrading and recycling damaged or defective cellular components. It plays a paradoxical role in GBM by either promoting or suppressing tumor growth depending on the cellular context. A thorough understanding of autophagy’s pleiotropic roles is needed to develop potential therapeutic strategies for GBM. In this paper, we discussed molecular mechanisms and biphasic functions of autophagy in gliomagenesis. We also provided a summary of treatments for GBM, emphasizing the importance of autophagy as a promising molecular target for treating GBM. MDPI 2021-06-06 /pmc/articles/PMC8227518/ /pubmed/34204169 http://dx.doi.org/10.3390/cells10061411 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Batara, Don Carlo Ramos
Choi, Moon-Chang
Shin, Hyeon-Uk
Kim, Hyunggee
Kim, Sung-Hak
Friend or Foe: Paradoxical Roles of Autophagy in Gliomagenesis
title Friend or Foe: Paradoxical Roles of Autophagy in Gliomagenesis
title_full Friend or Foe: Paradoxical Roles of Autophagy in Gliomagenesis
title_fullStr Friend or Foe: Paradoxical Roles of Autophagy in Gliomagenesis
title_full_unstemmed Friend or Foe: Paradoxical Roles of Autophagy in Gliomagenesis
title_short Friend or Foe: Paradoxical Roles of Autophagy in Gliomagenesis
title_sort friend or foe: paradoxical roles of autophagy in gliomagenesis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8227518/
https://www.ncbi.nlm.nih.gov/pubmed/34204169
http://dx.doi.org/10.3390/cells10061411
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