Epithelial to Mesenchymal Transition in Lung Cancer: Potential EMT-Targeting Natural Product-derived Compounds.


Journal

Anticancer research
ISSN: 1791-7530
Titre abrégé: Anticancer Res
Pays: Greece
ID NLM: 8102988

Informations de publication

Date de publication:
Sep 2022
Historique:
received: 20 06 2022
revised: 21 07 2022
accepted: 22 07 2022
entrez: 30 8 2022
pubmed: 31 8 2022
medline: 1 9 2022
Statut: ppublish

Résumé

Epithelial to mesenchymal transition (EMT) is the cellular transition process of epithelium-associated phenotypes and behaviors into mesenchymal phenotypes. EMT is linked with cancer, and it is believed to be an important factor facilitating the motility and invasive activity of solid tumor cells. EMT facilitates the capability of cancer cells to metastasize because it promotes cell survival in detached conditions and facilitates the establishment of new tumors. In lung cancer, EMT has garnered considerable attention because of its importance in metastasis and has been recognized as an important target for anticancer drug therapy. Several studies have pointed out the promising activities of natural product-derived compounds and other agents that have EMT-suppressive activities and may facilitate the development of novel strategies for lung cancer management. In this review, we discuss the recent discoveries regarding the fundamental signaling regulating EMT and identify molecular targets for anti-EMT activities of the natural product-derived compounds. We also highlight the anti-EMT effect of natural compounds with their molecular targets and mechanisms of action that may benefit the understanding of and support the development of EMT targeting therapy.

Identifiants

pubmed: 36039426
pii: 42/9/4237
doi: 10.21873/anticanres.15923
doi:

Substances chimiques

Biological Products 0

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

4237-4246

Informations de copyright

Copyright © 2022 International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.

Auteurs

Pithi Chanvorachote (P)

Center of Excellence in Cancer Cell and Molecular Biology, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, Thailand; pithi.c@chula.ac.th.
Department of Pharmacology and Physiology, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, Thailand.

Korrakod Petsri (K)

Center of Excellence in Cancer Cell and Molecular Biology, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, Thailand.
Department of Pharmacology and Physiology, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, Thailand.

Sunisa Thongsom (S)

Center of Excellence in Cancer Cell and Molecular Biology, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, Thailand.
Department of Pharmacology and Physiology, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok, Thailand.

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Classifications MeSH