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Extracellular-Signal Regulated Kinase: A Central Molecule Driving Epithelial–Mesenchymal Transition in Cancer

Authors
  • Olea-Flores, Monserrat1
  • Zuñiga-Eulogio, Miriam Daniela1
  • Mendoza-Catalán, Miguel Angel2
  • Rodríguez-Ruiz, Hugo Alberto2
  • Castañeda-Saucedo, Eduardo1
  • Ortuño-Pineda, Carlos2
  • Padilla-Benavides, Teresita3
  • Navarro-Tito, Napoleón1
  • 1 (E.C.-S.)
  • 2 (C.O.-P.)
  • 3 Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, USA
Type
Published Article
Journal
International Journal of Molecular Sciences
Publisher
MDPI AG
Publication Date
Jun 13, 2019
Volume
20
Issue
12
Identifiers
DOI: 10.3390/ijms20122885
PMID: 31200510
PMCID: PMC6627365
Source
PubMed Central
Keywords
License
Green

Abstract

Epithelial–mesenchymal transition (EMT) is a reversible cellular process, characterized by changes in gene expression and activation of proteins, favoring the trans-differentiation of the epithelial phenotype to a mesenchymal phenotype. This process increases cell migration and invasion of tumor cells, progression of the cell cycle, and resistance to apoptosis and chemotherapy, all of which support tumor progression. One of the signaling pathways involved in tumor progression is the MAPK pathway. Within this family, the ERK subfamily of proteins is known for its contributions to EMT. The ERK subfamily is divided into typical (ERK 1/2/5), and atypical (ERK 3/4/7/8) members. These kinases are overexpressed and hyperactive in various types of cancer. They regulate diverse cellular processes such as proliferation, migration, metastasis, resistance to chemotherapy, and EMT. In this context, in vitro and in vivo assays, as well as studies in human patients, have shown that ERK favors the expression, function, and subcellular relocalization of various proteins that regulate EMT, thus promoting tumor progression. In this review, we discuss the mechanistic roles of the ERK subfamily members in EMT and tumor progression in diverse biological systems.

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