ERK activation modulates invasiveness and Reactive Oxygen Species (ROS) production in triple negative breast cancer cell lines

Triple negative breast cancer (TNBC) is the breast cancer subtype with the worst prognosis and still lacks a targeted therapy. In this study, we found increased ERK phosphorylation in TNBC cell lines and an important role for ERK in sustaining the migration of TNBC cells. Although ROS have been sugg...

Full description

Saved in:
Bibliographic Details
Published in:Cellular signalling Vol. 101; p. 110487
Main Authors: Acosta-Casique, Adilene, Montes-Alvarado, José B., Barragán, Minuet, Larrauri-Rodríguez, Karen A., Perez-Gonzalez, Andrea, Delgado-Magallón, Alam, Millán-Perez-Peña, Lourdes, Rosas-Murrieta, Nora H., Maycotte, Paola
Format: Journal Article
Language:English
Published: England Elsevier Inc 01-01-2023
Subjects:
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Triple negative breast cancer (TNBC) is the breast cancer subtype with the worst prognosis and still lacks a targeted therapy. In this study, we found increased ERK phosphorylation in TNBC cell lines and an important role for ERK in sustaining the migration of TNBC cells. Although ROS have been suggested to have an important role in sustaining MAPK signaling, antioxidant treatment increased ERK phosphorylation, probably suggesting increased invasive potential. Interestingly, treatment with PD0325901 (PD), a MEK inhibitor, decreased ROS levels in TNBC cells and decreased mitochondrial fragmentation in the MDAMB231 cell line. Our data supports an important role for MEK/ERK in TNBC, sustaining cellular migration, regulating mitochondrial dynamics and ROS production in this breast cancer subtype. •We describe increased ERK phosphorylation in TNBC cell lines.•ERK showed an important role in sustaining cellular migration.•MEK/ERK in TNBC sustains cellular migration, regulating mitochondrial dynamics and ROS production.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0898-6568
1873-3913
DOI:10.1016/j.cellsig.2022.110487