衰老是一种细胞状态，其中细胞失去增殖能力，通常是不可逆转的。从生理学上来说，它的发生是由于与端粒缩短相关的细胞分裂能力有限，即所谓的复制衰老。 DNA 损伤、致癌激活、氧化应激或其他细胞成分损伤（统称为诱导衰老）也可能导致早期诱导衰老。肿瘤细胞获得了绕过复制衰老的能力，从而确保了复制的永生性，这是癌症的标志。然而，许多抗癌疗法会导致肿瘤细胞诱导衰老。最初，这种反应会导致肿瘤生长减慢。然而，由于构成衰老相关分泌表型（SASP）的众多分子和细胞外囊泡的富集，衰老细胞（SnC）在肿瘤中的长期积累可以促进肿瘤进展。除其他作用外，SASP 可以增强或释放肿瘤可塑性和表型转变，这是癌症的另一个标志。这篇综述讨论了 SnC 如何促进癌症可塑性的机制，如细胞分化、干性、重编程和上皮间质转化。我们还讨论了 SnC 抵抗细胞死亡的主要分子机制，以及针对 SnC 的潜在策略。最后，我们提出了该领域的开放性问题和临床相关观点。

Senescence is a cellular state in which the cell loses its proliferative capacity, often irreversibly. Physiologically, it occurs due to a limited capacity of cell division associated with telomere shortening, the so-called replicative senescence. It can also be induced early due to DNA damage, oncogenic activation, oxidative stress, or damage to other cellular components (collectively named induced senescence). Tumor cells acquire the ability to bypass replicative senescence, thus ensuring the replicative immortality, a hallmark of cancer. Many anti-cancer therapies, however, can lead tumor cells to induced senescence. Initially, this response leads to a slowdown in tumor growth. However, the longstanding accumulation of senescent cells (SnCs) in tumors can promote neoplastic progression due to the enrichment of numerous molecules and extracellular vesicles that constitutes the senescence-associated secretory phenotype (SASP). Among other effects, SASP can potentiate or unlock the tumor plasticity and phenotypic transitions, another hallmark of cancer. This review discusses how SnCs can fuel mechanisms that underlie cancer plasticity, like cell differentiation, stemness, reprogramming, and epithelial-mesenchymal transition. We also discuss the main molecular mechanisms that make SnCs resistant to cell death, and potential strategies to target SnCs. At the end, we raise open questions and clinically relevant perspectives in the field.