Autophagy as a mechanism for anti-angiogenic therapy resistance.
Angiogenesis
Anti-angiogenesis
Autophagy
Cancer
Drug resistance
VEGF
Journal
Seminars in cancer biology
ISSN: 1096-3650
Titre abrégé: Semin Cancer Biol
Pays: England
ID NLM: 9010218
Informations de publication
Date de publication:
11 2020
11 2020
Historique:
received:
21
01
2019
accepted:
27
08
2019
pubmed:
1
9
2019
medline:
2
9
2021
entrez:
1
9
2019
Statut:
ppublish
Résumé
Autophagy is a lysosomal-dependent degradation process that is highly conserved and maintains cellular homeostasis by sequestering cytosolic material for degradation either non-specifically by non-selective autophagy, or targeting specific proteins aggregates by selective autophagy. Autophagy serves as a protective mechanism defending the cell from stressors and also plays an important role in enabling tumor cells to overcome harsh conditions arising in their microenvironment during growth as well as oxidative and non-oxidative injuries secondary to therapeutic stressors. Recently, autophagy has been implicated to cause tumor resistance to anti-angiogenic therapy, joining an existing literature implicating autophagy in cancer resistance to conventional DNA damaging chemotherapy and ionizing radiation. In this review, we discuss the role of angiogenesis in malignancy, mechanisms of resistance to anti-angiogenic therapy in general, the role of autophagy in driving malignancy, and the current literature in autophagy-mediated anti-angiogenic therapy resistance. Finally, we provide future insight into the current challenges of using autophagy inhibitors in the clinic and provides tips for future studies to focus on to effectively target autophagy in overcoming resistance to anti-angiogenic therapy.
Identifiants
pubmed: 31472232
pii: S1044-579X(19)30014-8
doi: 10.1016/j.semcancer.2019.08.031
pmc: PMC7047534
mid: NIHMS1051244
pii:
doi:
Substances chimiques
Angiogenesis Inhibitors
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
75-88Subventions
Organisme : NCI NIH HHS
ID : R01 CA227136
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS079697
Pays : United States
Organisme : NCI NIH HHS
ID : T32 CA151022
Pays : United States
Informations de copyright
Copyright © 2019 Elsevier Ltd. All rights reserved.
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