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Updated: Aug 26, 2025

Quantification of Breast Cancer Cell Invasiveness Using a Three-dimensional 3D Model
Published on: June 11, 2014
ERK activation modulates invasiveness and Reactive Oxygen Species (ROS) production in triple negative breast cancer
Adilene Acosta-Casique1, José B Montes-Alvarado2, Minuet Barragán1
1Centro de Investigación Biomédica de Oriente (CIBIOR), Instituto Mexicano del Seguro Social (IMSS), Km 4.5 Carretera Atlixco-Metepec HGZ5, Puebla 74360, Mexico; Facultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla (BUAP), Ciudad Universitaria, Puebla 72570, Mexico.
Abstract:
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.
Insights
Triple negative breast cancer (TNBC) research reveals ERK pathway is crucial for cell migration and mitochondrial function. MEK inhibitor PD0325901 reduced reactive oxygen species and mitochondrial fragmentation in TNBC cells.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Triple negative breast cancer (TNBC) presents a poor prognosis and lacks targeted therapies.
- The mitogen-activated protein kinase (MAPK) signaling pathway, particularly ERK, is implicated in cancer progression.
Purpose of the Study:
- To investigate the role of the MEK/ERK pathway in TNBC.
- To explore the effects of MEK inhibition on TNBC cell migration, mitochondrial dynamics, and reactive oxygen species (ROS) production.
Main Methods:
- Analysis of ERK phosphorylation in TNBC cell lines.
- Assessment of TNBC cell migration.
- Evaluation of mitochondrial fragmentation and ROS levels following treatment with PD0325901 (a MEK inhibitor) and antioxidants.
Main Results:
- Elevated ERK phosphorylation was observed in TNBC cell lines, correlating with sustained cell migration.
- Antioxidant treatment paradoxically increased ERK phosphorylation, suggesting enhanced invasiveness.
- PD0325901 treatment decreased ROS levels and mitochondrial fragmentation in MDAMB231 cells.
Conclusions:
- The MEK/ERK pathway plays a significant role in TNBC.
- Targeting MEK/ERK may offer a therapeutic strategy for TNBC by impacting cell migration, mitochondrial function, and ROS production.
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