自噬被定义为“自我消化”的信号，是一种细胞死亡机制，其主要功能是降解有毒物质和老化细胞器，以确保细胞内的稳态。自噬的基本级别存在于细胞中，当其水平超过标准阈值时，会观察到细胞死亡诱导。在癌症中，自噬失调已经得到了充分的研究，特别是通过表观遗传因素，尤其是微型RNA（miRNA）对该通路的调节，这是一个值得注意的有趣点。miRNA被认为是不编码功能蛋白质的短内源性RNA，它们是细胞死亡通路（如凋亡、坏死，以及自噬）的重要调节因子。累积的数据表明，在肿瘤进程中，存在miRNA失调（上调或下调），它们的治疗性干预为癌症治疗提供了新的思路。miRNA/自噬在人类癌症中的作用已经得到了研究，一个令人兴奋的点是，自噬和miRNA都具有促癌和抑癌因子的双重功能。通过miRNA刺激促生存的自噬可以提高肿瘤细胞的存活率，并通过诱导EMT介导癌症转移。此外，通过miRNA诱导促死亡的自噬对肿瘤细胞的生存率产生负面影响，降低其生存率。miRNA/自噬轴的功能超出了调节肿瘤细胞的生长和入侵，它们还可以影响药物耐药性和放射耐药性。本文评述了最近实验提供的新的更新，涉及这些主题。版权所有© 2023作者。Elsevier Ltd.保留所有权利。

Autophagy is defined as a "self-digestion" signal, and it is a cell death mechanism its primary function is degrading toxic agents and aged organelles to ensure homeostasis in cells. The basic leve ls of autophagy are found in cells, and when its levels exceed to standard threshold, cell death induction is observed. Autophagy dysregulation in cancer has been well-documented, and regulation of this pathway by epigenetic factors, especially microRNAs (miRNAs), is interesting and noteworthy. miRNAs are considered short endogenous RNAs that do not encode functional proteins, and they are essential regulators of cell death pathways such as apoptosis, necroptosis, and autophagy. Accumulating data has revealed miRNA dysregulation (upregulation or downregulation) during tumor progression, and their therapeutic manipulation provides new insight into cancer therapy. miRNA/autophagy axis in human cancers has been investigated an exciting point is the dual function of both autophagy and miRNAs as oncogenic and onco-suppressor factors. The stimulation of pro-survival autophagy by miRNAs can increase the survival rate of tumor cells and mediates cancer metastasis via EMT inductionFurthermore, pro-death autophagy induction by miRNAs has a negative impact on the viability of tumor cells and decreases their survival rate. The miRNA/autophagy axis functions beyond regulating the growth and invasion of tumor cells, and they can also affect drug resistance and radio-resistance. These subjects are covered in the current review regarding the new updates provided by recent experiments.Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.