由肿瘤细胞及其相关肿瘤微环境（TME）组成的复杂肿瘤生态系统不断影响肿瘤行为，并最终影响治疗失败、疾病进展、复发和患者较差的总体生存率。肿瘤细胞和 TME 之间的串扰通过产生代谢变化（例如缺氧环境和营养波动）来放大复杂性。 TME 的这些变化在癌细胞中启动了类似干细胞的程序，有助于肿瘤异质性并增加肿瘤的稳健性。最近的研究表明，自噬在促进成纤维细胞产生、干性、癌细胞在较长休眠期的存活、转移性疾病的最终生长和抗病性方面发挥着多方面的作用。最近正在进行的研究将自噬/线粒体自噬作为一种强大的生存策略，以应对 TME 中的营养缺乏、缺氧和环境压力等环境压力。它可以防止不可逆的衰老，促进休眠的干细胞样状态，诱导上皮-间质转化并增加肿瘤细胞的迁移和侵袭潜力。本综述讨论了癌症干细胞（CSC）表型的自噬依赖性诱导背后的各种理论和机制。鉴于自噬功能在 CSC 侵袭性和治疗抵抗中的作用，讨论了基于通过阻断自噬抑制细胞可塑性作为杀死肿瘤细胞的强大治疗策略的各种机制和研究。

Complex tumour ecosystem comprising tumour cells and its associated tumour microenvironment (TME) constantly influence the tumoural behaviour and ultimately impact therapy failure, disease progression, recurrence and poor overall survival of patients. Crosstalk between tumour cells and TME amplifies the complexity by creating metabolic changes such as hypoxic environment and nutrient fluctuations. These changes in TME initiate stem cell-like programmes in cancer cells, contribute to tumoural heterogeneity and increase tumour robustness. Recent studies demonstrate the multifaceted role of autophagy in promoting fibroblast production, stemness, cancer cell survival during longer periods of dormancy, eventual growth of metastatic disease and disease resistance. Recent ongoing studies examine autophagy/mitophagy as a powerful survival strategy in response to environmental stress including nutrient deprivation, hypoxia and environmental stress in TME. It prevents irreversible senescence, promotes dormant stem-like state, induces epithelial-mesenchymal transition and increases migratory and invasive potential of tumour cells. The present review discusses various theories and mechanisms behind the autophagy-dependent induction of cancer stem cell (CSC) phenotype. Given the role of autophagic functions in CSC aggressiveness and therapeutic resistance, various mechanisms and studies based on suppressing cellular plasticity by blocking autophagy as a powerful therapeutic strategy to kill tumour cells are discussed.