Autophagy and epithelial mesenchymal transition (EMT) are critical processes in cancer progression. Autophagy, a cellular degradation process, and EMT, a mechanism where epithelial cells acquire mesenchymal features, both play significant roles in cancer development. This review explores the complex interactions between autophagy and EMT, particularly how autophagy influences cancer cell fate during EMT. The findings suggest that both autophagy and EMT are important targets for cancer therapy. Autophagy can promote DNA repair, cell adhesion, and proliferation, while EMT is involved in tumor invasion, metastasis, and resistance to therapy. Autophagy can either suppress or promote cancer depending on the context, acting as a tumor suppressor or pro-survival mechanism. Autophagy is regulated by various signaling pathways, including mTOR, AMPK, and TFEB. Autophagy plays a role in DNA repair and the DNA damage response (DDR), and its dysregulation can contribute to genomic instability. Autophagy is also involved in inflammation and cancer stem cell (CSC) maintenance, which are critical for tumor progression and therapy resistance. Targeting autophagy with drugs like hydroxychloroquine (HCQ) and combination therapies with other agents may offer new strategies for cancer treatment. EMT is a reversible process that facilitates tumor invasion and metastasis, and its regulation is crucial for cancer therapy. EMT-related transcription factors, such as Twist, Snail, and ZEB, promote drug resistance in cancer cells. Targeting EMT and autophagy may provide new approaches to overcome drug resistance and improve cancer treatment outcomes.Autophagy and epithelial mesenchymal transition (EMT) are critical processes in cancer progression. Autophagy, a cellular degradation process, and EMT, a mechanism where epithelial cells acquire mesenchymal features, both play significant roles in cancer development. This review explores the complex interactions between autophagy and EMT, particularly how autophagy influences cancer cell fate during EMT. The findings suggest that both autophagy and EMT are important targets for cancer therapy. Autophagy can promote DNA repair, cell adhesion, and proliferation, while EMT is involved in tumor invasion, metastasis, and resistance to therapy. Autophagy can either suppress or promote cancer depending on the context, acting as a tumor suppressor or pro-survival mechanism. Autophagy is regulated by various signaling pathways, including mTOR, AMPK, and TFEB. Autophagy plays a role in DNA repair and the DNA damage response (DDR), and its dysregulation can contribute to genomic instability. Autophagy is also involved in inflammation and cancer stem cell (CSC) maintenance, which are critical for tumor progression and therapy resistance. Targeting autophagy with drugs like hydroxychloroquine (HCQ) and combination therapies with other agents may offer new strategies for cancer treatment. EMT is a reversible process that facilitates tumor invasion and metastasis, and its regulation is crucial for cancer therapy. EMT-related transcription factors, such as Twist, Snail, and ZEB, promote drug resistance in cancer cells. Targeting EMT and autophagy may provide new approaches to overcome drug resistance and improve cancer treatment outcomes.