Drug induced resistance is a widespread problem in the clinical management of cancer. Cancer cells, when exposed to cytotoxic drugs, can reprogram their cellular machinery and resist cell death. Evasion of cell death mechanisms, such as apoptosis and necroptosis, are part of a transcriptional reprogramming that cancer cells utilize to mediate cytotoxic threats. An additional strategy adopted by cancer cells to resist cell death is to initiate the epithelial to mesenchymal transition (EMT) program. EMT is a trans-differentiation process which facilitates a motile phenotype in cancer cells which can be induced when cells are challenged by specific classes of cytotoxic drugs. Induction of EMT in malignant cells also results in drug resistance. In this setting, therapy-induced senescence (TIS), an enduring “proliferative arrest”, serves as an alternate approach against cancer because cancer cells remain susceptible to induced senescence. The molecular processes of senescence have proved challenging to understand. Senescence has previously been described solely as a tumor-suppressive mechanism; however, recent evidences suggest that senescence-associated secretory phenotype (SASP) can contribute to tumor progression. SASP has also been identified to contribute to EMT induction. Even though the causes of senescence and EMT induction can be wholly different from each other, a functional link between EMT and senescence is still obscure. In this review, we summarize the evidence of potential cross-talk between EMT and senescence while highlighting some of the most commonly identified molecular players. This review will shed light on these two intertwined and highly conserved cellular process, while providing background of the therapeutic implications of these processes.

药物诱导的耐药性是癌症临床治疗中普遍存在的问题。当癌细胞接触细胞毒性药物时，它们可以重新编程其细胞机制并抵抗细胞死亡。逃避细胞死亡机制，例如细胞凋亡和坏死性凋亡，是癌细胞用来介导细胞毒性威胁的转录重编程的一部分。癌细胞抵抗细胞死亡的另一种策略是启动上皮间质转化（EMT）程序。EMT 是一种转分化过程，可促进癌细胞的运动表型，当细胞受到特定类别的细胞毒性药物的攻击时，可以诱导这种运动表型。恶性细胞中 EMT 的诱导也会导致耐药性。在这种情况下，治疗诱导衰老（TIS），一种持久的“增殖停滞”，可以作为对抗癌症的替代方法，因为癌细胞仍然容易受到诱导衰老的影响。事实证明，衰老的分子过程很难理解。此前，衰老仅被描述为一种肿瘤抑制机制。然而，最近的证据表明衰老相关分泌表型（SASP）可能促进肿瘤进展。SASP 还被确定有助于 EMT 诱导。尽管衰老和 EMT 诱导的原因可能完全不同，但 EMT 和衰老之间的功能联系仍然不清楚。在这篇综述中，我们总结了 EMT 和衰老之间潜在交叉的证据，同时强调了一些最常见的分子参与者。这篇综述将阐明这两个相互交织且高度保守的细胞过程，同时提供这些过程的治疗意义的背景。