Autophagy Modulation by Viral Infections Influences Tumor Development

Abstract

Autophagy is a self-degradative process important for balancing cellular homeostasis at critical times in development and/or in response to nutrient stress. This is particularly relevant in tumor model in which autophagy has been demonstrated to have an important impact on tumor behavior. In one hand, autophagy limits tumor transformation of precancerous cells in early stage, and in the other hand, it favors the survival, proliferation, metastasis, and resistance to antitumor therapies in more advanced tumors. This catabolic machinery can be induced by an important variety of extra- and intracellular stimuli. For instance, viral infection has often been associated to autophagic modulation, and the role of autophagy in virus replication differs according to the virus studied. In the context of tumor development, virus-modulated autophagy can have an important impact on tumor cells’ fate. Extensive analyses have shed light on the molecular and/or functional complex mechanisms by which virus-modulated autophagy influences precancerous or tumor cell development. This review includes an overview of discoveries describing the repercussions of an autophagy perturbation during viral infections on tumor behavior.

mIR-99a-5p and mIR-148a-3p as Candidate Molecular Biomarkers for the Survival of Lung Cancer Patients

“…Shi et al, (2016) reported that knocking out HMGA2 increased the expression of pro-apoptotic genes Bax and reduced cell proliferation, indicating the anti-apoptotic ability of HMGA2 in cancer cells. A recent study by Leonardi et al, (2021) reported that CDK was dysregulated during virus infection to bypass the cell cycle in tumorigenesis. Thus, our target genes are consistent with enrichment in response to viruses and G1/S and G2/M transition of mitotic cell cycles.…”

“…KPNA4 is a nuclear import protein that is vital in promoting malignant phenotypes in LUAD cells (Hu et al, 2020). Both KPNA4 and KPNB1 were enriched in the modulation of the virus-mediated host process, and autophagy has been reported to influence tumour behaviour, especially at the early stages of oncogenesis (Leonardi et al, 2021). KARS encodes aminoacyl-tRNA synthetase, which is required for mRNA translation and has become a target of autoantibodies in autoimmune diseases (Vargas et al, 2020).…”

Viruses Binding to Host Receptors Interacts with Autophagy

“…However, what is interesting is that when a pathogen infects, autophagy is initiated to eliminate the pathogen. During virus replication, autophagy is activated to complete the replication of viruses by maintaining the state of the cell [ 52 ]. From the perspective of pathogens, it would be interesting to see how autophagy affects infections.…”

ThePI3K/AKTsignalling pathway in inflammation, cell death and glial scar formation after traumatic spinal cord injury: Mechanisms and therapeutic opportunities

“…Microautophagy refers to invagination of the lysosomal membrane for the phagocytosis of cytoplasmic substrates. Macroautophagy is characterized by the formation of autophagosomes with a double‐layered membrane structure; these autophagosomes fuse with lysosomes to form autophagolysosomes, which degrade and recycle the phagocytosed substances 99,100 . Macroautophagy is the most common form of autophagy (hereinafter, macroautophagy is referred to as autophagy); it can be activated by unc‐51‐like autophagy activating kinase 1 (ULK 1), ULK 2, autophagy‐related protein 13 (Atg13) and Beclin‐1/III PI3K complexes.…”

“…Macroautophagy is characterized by the formation of autophagosomes with a double-layered membrane structure; these autophagosomes fuse with lysosomes to form autophagolysosomes, which degrade and recycle the phagocytosed substances. 99,100 Macroautophagy is the most common form of autophagy (hereinafter, macroautophagy is referred to as autophagy); it can be activated by unc-51-like autophagy activating kinase 1 (ULK 1), ULK 2, autophagy-related protein 13 (Atg13) and Beclin-1/III PI3K complexes. When autophagy is activated, these complexes recruit other proteins involved in the extension and formation of autophagosomes (e.g., Atg12, Atg5, Atg16L and light chain 3 [LC3]) to form conjugate complexes.…”