Published online May 26, 2020. doi: 10.4252/wjsc.v12.i5.303
Peer-review started: February 27, 2020
First decision: April 7, 2020
Revised: April 19, 2020
Accepted: May 5, 2020
Article in press: May 5, 2020
Published online: May 26, 2020
Autophagy is a highly regulated catabolic process in which superfluous, damaged organelles and other cytoplasmic constituents are delivered to the lysosome for clearance and the generation of macromolecule substrates during basal or stressed conditions. Autophagy is a bimodal process with a context dependent role in the initiation and the development of cancers. For instance, autophagy provides an adaptive response to cancer stem cells to survive metabolic stresses, by influencing disease propagation via modulation of essential signaling pathways or by promoting resistance to chemotherapeutics. Autophagy has been implicated in a cross talk with apoptosis. Understanding the complex interactions provides an opportunity to improve cancer therapy and the clinical outcome for the cancer patients. In this review, we provide a comprehensive view on the current knowledge on autophagy and its role in cancer cells with a particular focus on cancer stem cell homeostasis.
Core tip: Cancer stem cells (CSCs) are a distinct subpopulation in the tumor bulk that are highly plastic, and autophagy has been suggested to modulate their stemness and development during cancer progression. Autophagy is a pro-survival mechanism used by cancer cells to provide bioenergetic substrates. Therefore, dissecting the role of autophagy in cancer propagation can theoretically lead to a more efficient cancer treatment via the modulation of autophagy, in combination with chemotherapeutics to sensitize and target CSCs. This review summarizes the divergent role of autophagy in CSCs and cancer cells and attempts to elucidate the molecular mechanisms involved.