Unit of Oncogenetics and Functional Oncogenomics, CRO Aviano, National Cancer Institute, IRCCS, I‑33081 Aviano, Italy.
Int J Oncol. 2024 Jun;64(6). doi: 10.3892/ijo.2024.5645. Epub 2024 Apr 12.
Autophagy is a conserved catabolic process that controls organelle quality, removes misfolded or abnormally aggregated proteins and is part of the defense mechanisms against intracellular pathogens. Autophagy contributes to the suppression of tumor initiation by promoting genome stability, cellular integrity, redox balance and proteostasis. On the other hand, once a tumor is established, autophagy can support cancer cell survival and promote epithelial‑to‑mesenchymal transition. A growing number of molecules involved in autophagy have been identified. In addition to their key canonical activity, several of these molecules, such as ATG5, ATG12 and Beclin‑1, also exert autophagy‑independent functions in a variety of biological processes. The present review aimed to summarize autophagy‑independent functions of molecules of the autophagy machinery and how the activity of these molecules can influence signaling pathways that are deregulated in cancer progression.
自噬是一种保守的分解代谢过程，可控制细胞器的质量，清除错误折叠或异常聚集的蛋白质，是抵御细胞内病原体的防御机制的一部分。自噬通过促进基因组稳定性、细胞完整性、氧化还原平衡和蛋白质稳态有助于抑制肿瘤的发生。另一方面，一旦肿瘤形成，自噬可以支持癌细胞的存活并促进上皮-间充质转化。越来越多的参与自噬的分子已被鉴定。除了它们的关键经典活性外，这些分子中的几种，如 ATG5、ATG12 和 Beclin-1，在各种生物过程中还发挥着自噬非依赖性的功能。本综述旨在总结自噬机制分子的非依赖性功能，以及这些分子的活性如何影响癌症进展中失调的信号通路。
