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Cellular senescence: a double-edged sword in cancer therapy

Over the past few decades, cellular senescence has been identified in cancer patients undergoing chemotherapy and radiotherapy. Senescent cells are generally characterized by permanent cell cycle arrest as a response to endogenous and exogenous stresses. In addition to exiting the cell cycle process...

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Autores principales: Xiao, Shuai, Qin, Dongmin, Hou, Xueyang, Tian, Lingli, Yu, Yeping, Zhang, Rui, Lyu, Hao, Guo, Dong, Chen, Xing-Zhen, Zhou, Cefan, Tang, Jingfeng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10522834/
https://www.ncbi.nlm.nih.gov/pubmed/37771436
http://dx.doi.org/10.3389/fonc.2023.1189015
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author Xiao, Shuai
Qin, Dongmin
Hou, Xueyang
Tian, Lingli
Yu, Yeping
Zhang, Rui
Lyu, Hao
Guo, Dong
Chen, Xing-Zhen
Zhou, Cefan
Tang, Jingfeng
author_facet Xiao, Shuai
Qin, Dongmin
Hou, Xueyang
Tian, Lingli
Yu, Yeping
Zhang, Rui
Lyu, Hao
Guo, Dong
Chen, Xing-Zhen
Zhou, Cefan
Tang, Jingfeng
author_sort Xiao, Shuai
collection PubMed
description Over the past few decades, cellular senescence has been identified in cancer patients undergoing chemotherapy and radiotherapy. Senescent cells are generally characterized by permanent cell cycle arrest as a response to endogenous and exogenous stresses. In addition to exiting the cell cycle process, cellular senescence also triggers profound phenotypic changes such as senescence-associated secretory phenotype (SASP), autophagy modulation, or metabolic reprograming. Consequently, cellular senescence is often considered as a tumor-suppressive mechanism that permanently arrests cells at risk of malignant transformation. However, accumulating evidence shows that therapy-induced senescence can promote epithelial-mesenchymal transition and tumorigenesis in neighboring cells, as well as re-entry into the cell cycle and activation of cancer stem cells, thereby promoting cancer cell survival. Therefore, it is particularly important to rapidly eliminate therapy-induced senescent cells in patients with cancer. Here we review the hallmarks of cellular senescence and the relationship between cellular senescence and cancer. We also discuss several pathways to induce senescence in tumor therapy, as well as strategies to eliminate senescent cells after cancer treatment. We believe that exploiting the intersection between cellular senescence and tumor cells is an important means to defeat tumors.
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spelling pubmed-105228342023-09-28 Cellular senescence: a double-edged sword in cancer therapy Xiao, Shuai Qin, Dongmin Hou, Xueyang Tian, Lingli Yu, Yeping Zhang, Rui Lyu, Hao Guo, Dong Chen, Xing-Zhen Zhou, Cefan Tang, Jingfeng Front Oncol Oncology Over the past few decades, cellular senescence has been identified in cancer patients undergoing chemotherapy and radiotherapy. Senescent cells are generally characterized by permanent cell cycle arrest as a response to endogenous and exogenous stresses. In addition to exiting the cell cycle process, cellular senescence also triggers profound phenotypic changes such as senescence-associated secretory phenotype (SASP), autophagy modulation, or metabolic reprograming. Consequently, cellular senescence is often considered as a tumor-suppressive mechanism that permanently arrests cells at risk of malignant transformation. However, accumulating evidence shows that therapy-induced senescence can promote epithelial-mesenchymal transition and tumorigenesis in neighboring cells, as well as re-entry into the cell cycle and activation of cancer stem cells, thereby promoting cancer cell survival. Therefore, it is particularly important to rapidly eliminate therapy-induced senescent cells in patients with cancer. Here we review the hallmarks of cellular senescence and the relationship between cellular senescence and cancer. We also discuss several pathways to induce senescence in tumor therapy, as well as strategies to eliminate senescent cells after cancer treatment. We believe that exploiting the intersection between cellular senescence and tumor cells is an important means to defeat tumors. Frontiers Media S.A. 2023-09-12 /pmc/articles/PMC10522834/ /pubmed/37771436 http://dx.doi.org/10.3389/fonc.2023.1189015 Text en Copyright © 2023 Xiao, Qin, Hou, Tian, Yu, Zhang, Lyu, Guo, Chen, Zhou and Tang https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Oncology
Xiao, Shuai
Qin, Dongmin
Hou, Xueyang
Tian, Lingli
Yu, Yeping
Zhang, Rui
Lyu, Hao
Guo, Dong
Chen, Xing-Zhen
Zhou, Cefan
Tang, Jingfeng
Cellular senescence: a double-edged sword in cancer therapy
title Cellular senescence: a double-edged sword in cancer therapy
title_full Cellular senescence: a double-edged sword in cancer therapy
title_fullStr Cellular senescence: a double-edged sword in cancer therapy
title_full_unstemmed Cellular senescence: a double-edged sword in cancer therapy
title_short Cellular senescence: a double-edged sword in cancer therapy
title_sort cellular senescence: a double-edged sword in cancer therapy
topic Oncology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10522834/
https://www.ncbi.nlm.nih.gov/pubmed/37771436
http://dx.doi.org/10.3389/fonc.2023.1189015
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