Cancers induced by gene mutation, deletion, and genome instability might be related to aging. With similar pathways of aging but distinct functions, senescence at the cellular level is an irreversible arrest of cell cycle. Senescence has long been believed as a barrier to restrict tumor expansion. However, more and more evidence has been shown that senescence inducers regulate epithelial-mesenchymal transition, stem cell self-renewal, inflammatory response, crosstalk with the oncogenic bypass signaling, and conversion of oncogene to tumor suppressor. Here we will discuss the most recent findings of the oncogenic aspects of senescence which crosstalk with multiple pathways in cancer progression.

中文翻译：

---

肿瘤促进癌症进展中的衰老方面。

由基因突变，缺失和基因组不稳定引起的癌症可能与衰老有关。具有相似的衰老途径但功能不同，细胞水平的衰老是细胞周期的不可逆止。长期以来人们一直认为衰老是限制肿瘤扩展的障碍。然而，越来越多的证据表明，衰老诱导因子调节上皮-间质转化，干细胞自我更新，炎症反应，与致癌旁路信号的串扰以及癌基因向肿瘤抑制因子的转化。在这里，我们将讨论衰老的致癌方面的最新发现，这些方面与癌症进展中的多种途径相串扰。