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Targeting ARID1A-Deficient Cancers: An Immune-Metabolic Perspective

Epigenetic remodeling and metabolic reprogramming, two well-known cancer hallmarks, are highly intertwined. In addition to their abilities to confer cancer cell growth advantage, these alterations play a critical role in dynamically shaping the tumor microenvironment and antitumor immunity. Recent s...

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Autores principales: Lebedev, Timofey, Kousar, Rubina, Patrick, Bbumba, Usama, Muhammad, Lee, Meng-Kuei, Tan, Ming, Li, Xing-Guo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10047504/
https://www.ncbi.nlm.nih.gov/pubmed/36980292
http://dx.doi.org/10.3390/cells12060952
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author Lebedev, Timofey
Kousar, Rubina
Patrick, Bbumba
Usama, Muhammad
Lee, Meng-Kuei
Tan, Ming
Li, Xing-Guo
author_facet Lebedev, Timofey
Kousar, Rubina
Patrick, Bbumba
Usama, Muhammad
Lee, Meng-Kuei
Tan, Ming
Li, Xing-Guo
author_sort Lebedev, Timofey
collection PubMed
description Epigenetic remodeling and metabolic reprogramming, two well-known cancer hallmarks, are highly intertwined. In addition to their abilities to confer cancer cell growth advantage, these alterations play a critical role in dynamically shaping the tumor microenvironment and antitumor immunity. Recent studies point toward the interplay between epigenetic regulation and metabolic rewiring as a potentially targetable Achilles’ heel in cancer. In this review, we explore the key metabolic mechanisms that underpin the immunomodulatory role of AT-rich interaction domain 1A (ARID1A), the most frequently mutated epigenetic regulator across human cancers. We will summarize the recent advances in targeting ARID1A-deficient cancers by harnessing immune-metabolic vulnerability elicited by ARID1A deficiency to stimulate antitumor immune response, and ultimately, to improve patient outcome.
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spelling pubmed-100475042023-03-29 Targeting ARID1A-Deficient Cancers: An Immune-Metabolic Perspective Lebedev, Timofey Kousar, Rubina Patrick, Bbumba Usama, Muhammad Lee, Meng-Kuei Tan, Ming Li, Xing-Guo Cells Review Epigenetic remodeling and metabolic reprogramming, two well-known cancer hallmarks, are highly intertwined. In addition to their abilities to confer cancer cell growth advantage, these alterations play a critical role in dynamically shaping the tumor microenvironment and antitumor immunity. Recent studies point toward the interplay between epigenetic regulation and metabolic rewiring as a potentially targetable Achilles’ heel in cancer. In this review, we explore the key metabolic mechanisms that underpin the immunomodulatory role of AT-rich interaction domain 1A (ARID1A), the most frequently mutated epigenetic regulator across human cancers. We will summarize the recent advances in targeting ARID1A-deficient cancers by harnessing immune-metabolic vulnerability elicited by ARID1A deficiency to stimulate antitumor immune response, and ultimately, to improve patient outcome. MDPI 2023-03-21 /pmc/articles/PMC10047504/ /pubmed/36980292 http://dx.doi.org/10.3390/cells12060952 Text en © 2023 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
Lebedev, Timofey
Kousar, Rubina
Patrick, Bbumba
Usama, Muhammad
Lee, Meng-Kuei
Tan, Ming
Li, Xing-Guo
Targeting ARID1A-Deficient Cancers: An Immune-Metabolic Perspective
title Targeting ARID1A-Deficient Cancers: An Immune-Metabolic Perspective
title_full Targeting ARID1A-Deficient Cancers: An Immune-Metabolic Perspective
title_fullStr Targeting ARID1A-Deficient Cancers: An Immune-Metabolic Perspective
title_full_unstemmed Targeting ARID1A-Deficient Cancers: An Immune-Metabolic Perspective
title_short Targeting ARID1A-Deficient Cancers: An Immune-Metabolic Perspective
title_sort targeting arid1a-deficient cancers: an immune-metabolic perspective
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10047504/
https://www.ncbi.nlm.nih.gov/pubmed/36980292
http://dx.doi.org/10.3390/cells12060952
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