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Nucleophagy—Implications for Microautophagy and Health
Open AccessReview

The Multifaceted Role of CMA in Glioma: Enemy or Ally?

1
Department of Pathophysiology and Transplantation, University of Milan, Via F.Cervi 93, Segrate, 20090 Milan, Italy
2
Institute of Molecular Bioimaging and Physiology, National Research Council (IBFM-CNR), Via F.Cervi 93, Segrate, 20090 Milan, Italy
*
Author to whom correspondence should be addressed.
Authors contributed equally to this work.
Academic Editor: Masahide Oku
Int. J. Mol. Sci. 2021, 22(4), 2217; https://doi.org/10.3390/ijms22042217
Received: 30 January 2021 / Revised: 18 February 2021 / Accepted: 20 February 2021 / Published: 23 February 2021
(This article belongs to the Special Issue Microautophagy)
Chaperone-mediated autophagy (CMA) is a catabolic pathway fundamental for cell homeostasis, by which specific damaged or non-essential proteins are degraded. CMA activity has three main levels of regulation. The first regulatory level is based on the targetability of specific proteins possessing a KFERQ-like domain, which can be recognized by specific chaperones and delivered to the lysosomes. Target protein unfolding and translocation into the lysosomal lumen constitutes the second level of CMA regulation and is based on the modulation of Lamp2A multimerization. Finally, the activity of some accessory proteins represents the third regulatory level of CMA activity. CMA’s role in oncology has not been fully clarified covering both pro-survival and pro-death roles in different contexts. Taking all this into account, it is possible to comprehend the actual complexity of both CMA regulation and the cellular consequences of its activity allowing it to be elected as a modulatory and not only catabolic machinery. In this review, the role covered by CMA in oncology is discussed with a focus on its relevance in glioma. Molecular correlates of CMA importance in glioma responsiveness to treatment are described to identify new early efficacy biomarkers and new therapeutic targets to overcome resistance. View Full-Text
Keywords: PHLPP1; oxidative stress; autophagy; Temozolomide (TMZ); Hypoxia Inducible Factor-1α (HIF-1α); chaperone proteins; therapeutic target PHLPP1; oxidative stress; autophagy; Temozolomide (TMZ); Hypoxia Inducible Factor-1α (HIF-1α); chaperone proteins; therapeutic target
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MDPI and ACS Style

Lo Dico, A.; Martelli, C.; Diceglie, C.; Ottobrini, L. The Multifaceted Role of CMA in Glioma: Enemy or Ally? Int. J. Mol. Sci. 2021, 22, 2217. https://doi.org/10.3390/ijms22042217

AMA Style

Lo Dico A, Martelli C, Diceglie C, Ottobrini L. The Multifaceted Role of CMA in Glioma: Enemy or Ally? International Journal of Molecular Sciences. 2021; 22(4):2217. https://doi.org/10.3390/ijms22042217

Chicago/Turabian Style

Lo Dico, Alessia; Martelli, Cristina; Diceglie, Cecilia; Ottobrini, Luisa. 2021. "The Multifaceted Role of CMA in Glioma: Enemy or Ally?" Int. J. Mol. Sci. 22, no. 4: 2217. https://doi.org/10.3390/ijms22042217

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