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RESEARCH PAPER / 2026-02-12

Cellular senescence in cancer: Friend or fraud?

Qingxin Chen, Jianxin Liu, Jianming Wu, Xin Xiang, Xiaogang Zhou, Jianing Mi, Jing Wei, Xiao Zou, Anguo Wu

Sichuan Key Medical Laboratory of New Drug Discovery and Drugability Evaluation, Department of Cardiology, the Affiliated Hospital of Southwest Medical University and Key Laboratory of Medical Electrophysiology, Southwest Medical University, Luzhou, Sichuan 646000, China. Electronic address: [email protected]. · pubmed

Abstract

Cellular senescence, a stress-induced state of stable cell cycle arrest accompanied by a senescence-associated secretory phenotype (SASP), plays a paradoxical role in cancer biology. On the one hand, senescent cells function as a barrier to tumor initiation by activating the DNA damage response (DDR) and tumor suppressor pathways such as p53/p21 and p16

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

Cellular senescence can act as a barrier to tumor initiation through the activation of tumor suppressor pathways. The paper discusses mechanisms that could potentially be targeted to mitigate aging-related processes in cancer, aligning with longevity research.

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