Besides 2-methoxy-17beta-estradiol, cell cycle arrest via chromatin deacetylation can mitigate cell proliferation by decreasing global transcription while promoting the expression of tumor suppressor genes like p16INK4a while DNA Damage Repair (DDR) from pro-inflammatory cytokine production from senescent cells and Th1 lymphocytes can inhibit commitment to mitosis and cytokinesis by generating the paracrine SASP paradigm.
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Cancer Metastasis Rev. 2020; 39(3): 681–709