Apoptosis-Induced Compensatory Proliferation in Cancer

Ulisses Moreno-Celis, T. García-Gasca, C. Mejía
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引用次数: 4

Abstract

Apoptosis is a biological process that allows adequate cellular turnover and the elimination of damaged or infected cells. However, there are compensatory molecular mechanisms that promote cell proliferation after increased apoptotic events. These events are commonly mediated by mitogenic proteins, released by apoptotic cells, and received by neighboring cells, that trigger mechanisms similar to cell repair after an injury or traumatic event. This Note to the Reader: This chapter is part of the book Metastasis (ISBN: 978-0-6453320-2-5), scheduled for publication in April 2022. The book is being published by Exon Publications , Brisbane, Australia, and edited by Professor Consolato M. Segi, MD, PhD, MPH, FRCPC, FCAP, Anatomic Pathology Division, Children's Hospital of Eastern Ontario, ON, Canada. This chapter was published under the Rapid Publication service. It effect is known as "apoptosis-induced proliferation". This chapter addresses the process of apoptosis-induced proliferation, the regulatory mechanisms, and its importance in cancer development, progression, and therapy development. protein CCN1 suppresses hepatocarcinogenesis by inhibiting compensatory proliferation. Oncogene.
肿瘤细胞凋亡诱导的代偿性增殖
细胞凋亡是一种生物学过程,它允许足够的细胞更新和消除受损或感染的细胞。然而,在凋亡事件增加后,有代偿性分子机制促进细胞增殖。这些事件通常由有丝分裂蛋白介导,由凋亡细胞释放,并由邻近细胞接收,其触发机制类似于损伤或创伤事件后的细胞修复。本章是《转移》一书的一部分(ISBN: 978-0-6453320-2-5),计划于2022年4月出版。该书由澳大利亚布里斯班的Exon出版社出版,由Consolato M. Segi教授编辑,他是医学博士、公共卫生硕士、FRCPC、FCAP、加拿大安大略省东部儿童医院解剖病理学部。本章是在快速出版服务下出版的。这种效应被称为“细胞凋亡诱导增殖”。本章阐述了细胞凋亡诱导增殖的过程、调控机制及其在癌症发生、进展和治疗发展中的重要性。CCN1蛋白通过抑制代偿性增殖抑制肝癌的发生。致癌基因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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