Proteomics Laboratory, Indian Institute of Toxicology Research, (Council of Scientific & Industrial Research), PO Box 80, MG Marg, Lucknow-226001, India.
Cell Div. 2010 Jan 21;5:4. doi: 10.1186/1747-1028-5-4.
Senescence and mitotic catastrophe (MC) are two distinct crucial non-apoptotic mechanisms, often triggered in cancer cells and tissues in response to anti-cancer drugs. Chemotherapeuticals and myriad other factors induce cell eradication via these routes. While senescence drives the cells to a state of quiescence, MC drives the cells towards death during the course of mitosis. The senescent phenotype distinguishes tumor cells that survived drug exposure but lost the ability to form colonies from those that recover and proliferate after treatment. Although senescent cells do not proliferate, they are metabolically active and may secrete proteins with potential tumor-promoting activities. The other anti-proliferative response of tumor cells is MC that is a form of cell death that results from abnormal mitosis and leads to the formation of interphase cells with multiple micronuclei. Different classes of cytotoxic agents induce MC, but the pathways of abnormal mitosis differ depending on the nature of the inducer and the status of cell-cycle checkpoints. In this review, we compare the two pathways and mention that they are activated to curb the growth of tumors. Altogether, we have highlighted the possibilities of the use of senescence targeting drugs, mitotic kinases and anti-mitotic agents in fabricating novel strategies in cancer control.
衰老和有丝分裂灾难（MC）是两种截然不同的关键非凋亡机制，通常在癌细胞和组织中对抗癌药物产生反应时被触发。化疗药物和无数其他因素通过这些途径诱导细胞消除。虽然衰老使细胞进入静止状态，但 MC 在有丝分裂过程中使细胞走向死亡。衰老表型将经历药物暴露但丧失形成集落能力的存活肿瘤细胞与那些在治疗后恢复和增殖的细胞区分开来。虽然衰老细胞不再增殖，但它们具有代谢活性并且可能分泌具有潜在肿瘤促进活性的蛋白质。肿瘤细胞的另一种抗增殖反应是 MC，这是一种由于异常有丝分裂导致的细胞死亡形式，导致形成具有多个微核的间期间期细胞。不同类别的细胞毒性剂诱导 MC，但异常有丝分裂的途径因诱导剂的性质和细胞周期检查点的状态而异。在这篇综述中，我们比较了这两种途径，并指出它们被激活以抑制肿瘤的生长。总的来说，我们强调了使用衰老靶向药物、有丝分裂激酶和抗有丝分裂剂来制定癌症控制新策略的可能性。
