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Chinese Journal of Endourology(Electronic Edition) ›› 2024, Vol. 18 ›› Issue (05): 425-434. doi: 10.3877/cma.j.issn.1674-3253.2024.05.002

• Expert Forum • Previous Articles    

The mechanisms of senescence-associated secretory phenotype factors in the occurrence and progression of prostate cancer

Siping Hu1, Xingyu Xiong1, Hang Xu2, Lu Yang2,()   

  1. 1. Department of Urology, West China Hospital of Sichuan University, Chengdu 610041, China; West China School of Clinical Medicine of Sichuan University, Chengdu 610041, China
    2. Department of Urology, West China Hospital of Sichuan University, Chengdu 610041, China
  • Received:2024-03-29 Online:2024-10-01 Published:2024-09-19
  • Contact: Lu Yang

Abstract:

Cell senescence is triggered by stress damage or physiological processes. Senescence-associated secretory phenotype (SASP) is an important manifestation of cell senescence. SASP factors in prostate cancer and normal prostate include interleukins (IL-1, IL-6), chemokines (CXCL-8, GRO-a), matrix metalloproteinase (MMP) family, TNF-α, and intercellular adhesion molecule-1 (ICAM-1). P53, IL-1α, KDM4, ATM/HIF1α, ATM/TRAF6, and MTORC1 all regulate SASP. Endocrine therapy, radiotherapy, and chemotherapy can all induce cell senescence and lead to SASP. The role of SASP factor in prostate cancer cells is still not fully understood. Although many studies have shown that SASP factor plays an important role in prostate cancer cell survival, growth and proliferation, angiogenesis, metastasis, disease progression, and treatment resistance, there are still inconsistencies in existing results. SASP factor also has inhibitory and promoting effects on immune response. And SASP factor has shown potential anti-tumor effects in other malignant tumors. In addition, inducing prostate cancer cell senescence is a potential anti-cancer strategy, and multiple molecules can exert tumor inhibitory effects by inducing prostate cancer cell senescence. However, studies have shown that SASP factor induces PNT2 immortalized prostate cell senescence, but does not induce prostate cancer cell senescence. Given that the role of SASP factors in prostate cancer is not fully understood, and existing clinical research on SASP factor targeted therapy is still insufficient, further research on SASP factor related studies should be strengthened in the future.

Key words: Prostate cancer, Senescence-associated secretory phenotype (SASP), Apoptosis, Proliferation, Androgen receptor (AR), Tumor immunity, Epithelial mesenchymal transition, Bone metastasis, Neuroendocrine, Neutrophil extracellular trap, Cellular senescence

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