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. 2022 Dec 15;12:200. doi: 10.1186/s13578-022-00941-0

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Molecular pathways of senescence-inducing therapies of PCa. Several applied therapies including radiotherapy, chemotherapy and androgen receptor (AR) targeted therapy (androgen deprivation therapy, ADT; supraphysiological androgen level, SAL; AR antagonists). Radiotherapy and chemotherapy lead to persistent DNA damage which triggers ATM or ATR signaling and finally p53 and p21^WAF1/CIP1 activation. p21^WAF1/CIP1 inhibits CDKs and mediates senescence through hypophosphorylation of pRb. In addition, chemotherapy induces senescence through ROS-ERK-ETS-p16^INK4a and the p27^Kip1-pRb pathway. SAL mediates senescence by the p15^INK4b-p16^INK4a-pRb-E2F1 pathway. AR antagonists induce senescence through p15^INK4b-p16^INK4a. Senescent cells secrete many cytokines, growth factors and exosomes, known as senescence-associated secretory phenotype (SASP). These factors exert different autocrine/paracrine effects on the surrounding tumor microenvironment thereby promoting or inhibiting tumor growth (created in Biorender.com)