Laboratory of Enzymatic Degradation of Organic Compounds, G.K. Skryabin Institute of Biochemistry and Physiology of Microorganisms of RAS, Federal Research Center, Pushchino Center for Biological Research of the Russian Academy of Sciences, Prospekt Nauki 5, Pushchino, Moscow Region, 142290, Russia.
Department of Biochemistry and Molecular Medicine and CRCHUM, Université de Montréal, C.P. 6128, Succ. Centre-Ville, Montréal, Québec, H3C 3J7, Canada.
Semin Cancer Biol. 2022 Jun;81:48-53. doi: 10.1016/j.semcancer.2020.12.017. Epub 2020 Dec 26.
Senescence is a tumor suppressor response that prevents the proliferation of mutated cells and alert the immune system for their elimination. However, this program is not perfect and with time additional genetic and epigenetic changes can impair tumor suppression and promote cancer progression both in cell autonomous and non-cell autonomous manners. A polyploid barrier is implemented in senescent cells to further prevent cell expansion but polyploid cells can generate highly malignant tumor cells via de-polyploidization. The nuclear lamina can act as an additional fail safe to prevent cancer in these cells and drugs able to stabilize the nuclear lamina may help to treat cancers by preventing senescence escape.
衰老（Senescence）是一种肿瘤抑制反应，可防止突变细胞的增殖，并激活免疫系统将其清除。然而，该程序并不完美，随着时间的推移，其他遗传和表观遗传变化可能会损害肿瘤抑制作用，并以细胞自主和非细胞自主的方式促进癌症进展。衰老细胞中实施了多倍体障碍（polyploid barrier）以进一步防止细胞扩张，但多倍体细胞可以通过去多倍体化（de-polyploidization）产生高度恶性的肿瘤细胞。核纤层（nuclear lamina）可以作为额外的失效保护装置，以防止这些细胞发生癌变，而能够稳定核纤层的药物可能有助于通过防止衰老逃逸来治疗癌症。
