» Articles » PMID: 38398197

Contribution of Autophagy to Epithelial Mesenchymal Transition Induction During Cancer Progression

Overview
Journal Cancers (Basel)
Publisher MDPI
Specialty Oncology
Date 2024 Feb 24
PMID 38398197
Authors
Affiliations
Soon will be listed here.
Abstract

Epithelial Mesenchymal Transition (EMT) is a dedifferentiation process implicated in many physio-pathological conditions including tumor transformation. EMT is regulated by several extracellular mediators and under certain conditions it can be reversible. Autophagy is a conserved catabolic process in which intracellular components such as protein/DNA aggregates and abnormal organelles are degraded in specific lysosomes. In cancer, autophagy plays a controversial role, acting in different conditions as both a tumor suppressor and a tumor-promoting mechanism. Experimental evidence shows that deep interrelations exist between EMT and autophagy-related pathways. Although this interplay has already been analyzed in previous studies, understanding mechanisms and the translational implications of autophagy/EMT need further study. The role of autophagy in EMT is not limited to morphological changes, but activation of autophagy could be important to DNA repair/damage system, cell adhesion molecules, and cell proliferation and differentiation processes. Based on this, both autophagy and EMT and related pathways are now considered as targets for cancer therapy. In this review article, the contribution of autophagy to EMT and progression of cancer is discussed. This article also describes the multiple connections between EMT and autophagy and their implication in cancer treatment.

Citing Articles

Deciphering the Role of Cancer Stem Cells: Drivers of Tumor Evolution, Therapeutic Resistance, and Precision Medicine Strategies.

El-Tanani M, Rabbani S, Satyam S, Rangraze I, Wali A, El-Tanani Y Cancers (Basel). 2025; 17(3).

PMID: 39941751 PMC: 11815874. DOI: 10.3390/cancers17030382.


Targeting autophagy to enhance chemotherapy and immunotherapy in oral cancer.

Zeng X, Chen Y, Wang J, He M, Qiu J, Huang Y Front Immunol. 2025; 15():1535649.

PMID: 39840028 PMC: 11747659. DOI: 10.3389/fimmu.2024.1535649.


Curcumin enhances ATG3-dependent autophagy and inhibits metastasis in cervical carcinoma.

Zheng F, Lu J, Wang C, Yu H, Fu Y, Ma D Cell Div. 2024; 19(1):33.

PMID: 39609925 PMC: 11606299. DOI: 10.1186/s13008-024-00138-6.


The role of epithelial-mesenchymal transition in pulmonary fibrosis: lessons from idiopathic pulmonary fibrosis and COVID-19.

Niayesh-Mehr R, Kalantar M, Bontempi G, Montaldo C, Ebrahimi S, Allameh A Cell Commun Signal. 2024; 22(1):542.

PMID: 39538298 PMC: 11558984. DOI: 10.1186/s12964-024-01925-y.


Interconnection of CD133 Stem Cell Marker with Autophagy and Apoptosis in Colorectal Cancer.

Sipos F, Muzes G Int J Mol Sci. 2024; 25(20).

PMID: 39456981 PMC: 11508732. DOI: 10.3390/ijms252011201.


References
1.
Shi J, Guo C, Li Y, Ma J . The long noncoding RNA TINCR promotes self-renewal of human liver cancer stem cells through autophagy activation. Cell Death Dis. 2022; 13(11):961. PMC: 9668904. DOI: 10.1038/s41419-022-05424-1. View

2.
Xi H, Wang S, Wang B, Hong X, Liu X, Li M . The role of interaction between autophagy and apoptosis in tumorigenesis (Review). Oncol Rep. 2022; 48(6). PMC: 9579747. DOI: 10.3892/or.2022.8423. View

3.
Colella B, Faienza F, Carinci M, DAlessandro G, Catalano M, Santoro A . Autophagy induction impairs Wnt/β-catenin signalling through β-catenin relocalisation in glioblastoma cells. Cell Signal. 2018; 53:357-364. DOI: 10.1016/j.cellsig.2018.10.017. View

4.
Chockley P, Keshamouni V . Immunological Consequences of Epithelial-Mesenchymal Transition in Tumor Progression. J Immunol. 2016; 197(3):691-8. PMC: 4955875. DOI: 10.4049/jimmunol.1600458. View

5.
Debnath J, Gammoh N, Ryan K . Autophagy and autophagy-related pathways in cancer. Nat Rev Mol Cell Biol. 2023; 24(8):560-575. PMC: 9980873. DOI: 10.1038/s41580-023-00585-z. View