Targeting compensatory proliferation signals in oral cancer

Apoptosis is an orchestrated phenomenon that regulates cell populations in physiological and pathological conditions. Carcinogenesis involves a state of disequilibrium between cell proliferation and cell death. The resistance to conventional therapeutic modalities of cancer, including surgery, radio...

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Main Authors: Loganathan Kavitha, Vijayashree Priyadharsini J, Anitha P, Paramasivam A
Format: Article
Language:English
Published: Elsevier 2024-07-01
Series:Journal of Oral Biology and Craniofacial Research
Online Access:http://www.sciencedirect.com/science/article/pii/S2212426824000927
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author Loganathan Kavitha
Vijayashree Priyadharsini J
Anitha P
Paramasivam A
author_facet Loganathan Kavitha
Vijayashree Priyadharsini J
Anitha P
Paramasivam A
author_sort Loganathan Kavitha
collection DOAJ
description Apoptosis is an orchestrated phenomenon that regulates cell populations in physiological and pathological conditions. Carcinogenesis involves a state of disequilibrium between cell proliferation and cell death. The resistance to conventional therapeutic modalities of cancer, including surgery, radiotherapy, and chemotherapy, can be explained by the compensatory repair and regeneration that occurs in the tumor microenvironment following apoptosis through the apoptotic compensatory proliferation signaling microvesicles (ACPSVs) or apoptotic extracellular microvesicles (ApoEVs). These microvesicles provide proliferative signals and act as mutagens, triggering cell proliferation, angiogenesis, immune evasion, metastasis, and invasion. This review discusses the phenomenon of apoptosis-induced proliferation and the role of ApoEVs in establishing an oncoregenerative niche, resulting in therapeutic resistance and recurrence of malignancies.
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institution Kabale University
issn 2212-4268
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publishDate 2024-07-01
publisher Elsevier
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series Journal of Oral Biology and Craniofacial Research
spelling doaj-art-d9451b0afd754075a33c8c6282d134372025-01-24T04:45:06ZengElsevierJournal of Oral Biology and Craniofacial Research2212-42682024-07-01144461464Targeting compensatory proliferation signals in oral cancerLoganathan Kavitha0Vijayashree Priyadharsini J1Anitha P2Paramasivam A3Department of Oral and Maxillofacial Pathology, Ragas Dental College and Hospital (Affiliated to The Tamil Nadu Dr. MGR Medical University), ECR, Uthandi, Chennai-600119, IndiaClinical Genetics Lab, Centre for Cellular and Molecular Research (The Blue Lab), Saveetha Dental College & Hospital, Saveetha Institute of Medical and Technical Sciences [SIMATS], Saveetha University, Poonamallee High Road, Chennai, Tamil Nadu, 600077, India; Corresponding author.Clinical Genetics Lab, Centre for Cellular and Molecular Research (The Blue Lab), Saveetha Dental College & Hospital, Saveetha Institute of Medical and Technical Sciences [SIMATS], Saveetha University, Poonamallee High Road, Chennai, Tamil Nadu, 600077, IndiaMolecular Biology Lab, Centre for Cellular and Molecular Research (The Blue Lab), Saveetha Dental College & Hospital, Saveetha Institute of Medical and Technical Sciences [SIMATS], Saveetha University, Poonamallee High Road, Chennai, Tamil Nadu, 600077, IndiaApoptosis is an orchestrated phenomenon that regulates cell populations in physiological and pathological conditions. Carcinogenesis involves a state of disequilibrium between cell proliferation and cell death. The resistance to conventional therapeutic modalities of cancer, including surgery, radiotherapy, and chemotherapy, can be explained by the compensatory repair and regeneration that occurs in the tumor microenvironment following apoptosis through the apoptotic compensatory proliferation signaling microvesicles (ACPSVs) or apoptotic extracellular microvesicles (ApoEVs). These microvesicles provide proliferative signals and act as mutagens, triggering cell proliferation, angiogenesis, immune evasion, metastasis, and invasion. This review discusses the phenomenon of apoptosis-induced proliferation and the role of ApoEVs in establishing an oncoregenerative niche, resulting in therapeutic resistance and recurrence of malignancies.http://www.sciencedirect.com/science/article/pii/S2212426824000927
spellingShingle Loganathan Kavitha
Vijayashree Priyadharsini J
Anitha P
Paramasivam A
Targeting compensatory proliferation signals in oral cancer
Journal of Oral Biology and Craniofacial Research
title Targeting compensatory proliferation signals in oral cancer
title_full Targeting compensatory proliferation signals in oral cancer
title_fullStr Targeting compensatory proliferation signals in oral cancer
title_full_unstemmed Targeting compensatory proliferation signals in oral cancer
title_short Targeting compensatory proliferation signals in oral cancer
title_sort targeting compensatory proliferation signals in oral cancer
url http://www.sciencedirect.com/science/article/pii/S2212426824000927
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AT vijayashreepriyadharsinij targetingcompensatoryproliferationsignalsinoralcancer
AT anithap targetingcompensatoryproliferationsignalsinoralcancer
AT paramasivama targetingcompensatoryproliferationsignalsinoralcancer