Crosstalk between autophagy and microbiota in cancer progression

Abstract

Autophagy is a highly conserved catabolic process seen in eukaryotes and is essentially a lysosome-dependent protein degradation pathway. The dysregulation of autophagy is often associated with the pathogenesis of numerous types of cancers, and can not only promote the survival of cancer but also trigger the tumor cell death. During cancer development, the microbial community might predispose cells to tumorigenesis by promoting mucosal inflammation, causing systemic disorders, and may also regulate the immune response to cancer. The complex relationship between autophagy and microorganisms can protect the body by activating the immune system. In addition, autophagy and microorganisms can crosstalk with each other in multifaceted ways to influence various physiological and pathological responses involved in cancer progression. Various molecular mechanisms, correlating the microbiota disorders and autophagy activation, control the outcomes of protumor or antitumor responses, which depend on the cancer type, tumor microenvironment and disease stage. In this review, we mainly emphasize the leading role of autophagy during the interaction between pathogenic microorganisms and human cancers and investigate the various molecular mechanisms by which autophagy modulates such complicated biological processes. Moreover, we also highlight the possibility of curing cancers with multiple molecular agents targeting the microbiota/autophagy axis. Finally, we summarize the emerging clinical trials investigating the therapeutic potential of targeting either autophagy or microbiota as anticancer strategies, although the crosstalk between them has not been explored thoroughly.

Autophagy-associated circRNA circATG7 facilitates autophagy and promotes pancreatic cancer progression

“…Accumulated researches brought forward that the crosstalk between circRNAs and autophagy probably exert essential function involving in the tumor development [ 27 , 28 ]. Meanwhile, appropriate degree of autophagy can promote the physiological homeostasis of tumor cells, and mediate cell protection by degrading proteins, organelles, or metabolites [ 29 ]. Therefore, clarifying the correlation of circRNAs and autophagy seems particularly important to the research about pancreatic cancer.…”

Editorial: The interactions between gastrointestinal microbiota and Helicobacter pylori in diseases

“…Autophagy is a highly conserved catabolic process, which plays a double-edge role in cancer progression (Wang et al, 2021). Yang et al presented an overview of autophagy in H. pylori infection and related GC with the focus on the relationship between H. pylori virulence factors and autophagy, core autophagy protein markers associated with H. pylori infection, the autophagy mediated signaling pathways involved in H. pylori-associated GC and potential drugs therapy targeting autophagy.…”

“…Autophagy is a highly conserved catabolic process, which plays a double-edge role in cancer progression ( Wang et al., 2021 ). Yang et al.…”

Progress of Autophagy in Epilepsy Research

“…Under physiological stress, autophagy mediates the clearance of misfolded, ubiquitinated proteins or damaged organelles, such as selective removal of mitochondria by autophagy to adapt to hunger [12], tumor inhibition [13], antigen presentation [14] and so on. In the pathological process, autophagy damage is also associated with a variety of human diseases, such as cancer [15], heart disease [16], autoimmune diseases [17] and nervous system diseases [18], including epilepsy [5]. In addition, autophagy is also considered as a target for the treatment of nervous system diseases.…”