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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Format: | Article |
Language: | English |
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Elsevier
2024-07-01
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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. |
format | Article |
id | doaj-art-d9451b0afd754075a33c8c6282d13437 |
institution | Kabale University |
issn | 2212-4268 |
language | English |
publishDate | 2024-07-01 |
publisher | Elsevier |
record_format | Article |
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 |
work_keys_str_mv | AT loganathankavitha targetingcompensatoryproliferationsignalsinoralcancer AT vijayashreepriyadharsinij targetingcompensatoryproliferationsignalsinoralcancer AT anithap targetingcompensatoryproliferationsignalsinoralcancer AT paramasivama targetingcompensatoryproliferationsignalsinoralcancer |