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Updated: Feb 14, 2026
09:29
Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
Published on: March 20, 2020
19.0K
Dissecting Context-Specific Effects of ERK5 Signaling in Triple-Negative Breast Cancer.
Katherine L Hebert1, Sarah B Knopf1, Thomas Cheng1
1Department of Medicine, Section of Hematology & Medical Oncology, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Cancers
|February 13, 2026
Summary
Extracellular signal-regulated kinase 5 (ERK5) impacts triple-negative breast cancer (TNBC) progression by regulating the tumor microenvironment and cell motility. Targeting ERK5 may offer new therapeutic strategies for aggressive TNBC.
Area of Science:
- Cancer Biology
- Molecular Oncology
- Biomedical Engineering
Background:
- Triple-negative breast cancer (TNBC) is an aggressive subtype with limited treatment options and poor outcomes.
- Identifying novel druggable targets is crucial for improving TNBC therapy response.
- Extracellular signal-regulated kinase 5 (ERK5) plays a role in cancer progression, including TNBC extracellular matrix interactions.
Purpose of the Study:
- To characterize the impact of ERK5 on triple-negative breast cancer (TNBC) biology using 2D culture, 3D spheroids, and a 3D breast adipose-macrophysiological system (BA-MaPS).
- To investigate ERK5's role in TNBC cell migration, gene expression, and tumor microenvironment remodeling.
Main Methods:
- Assessed TNBC cell migration (MDA-MB-231 parental vs. ERK5-knockout) using transwell, scratch, and spheroid pseudo-migration assays across three in vitro models.
- Performed RNA sequencing and pathway analysis to identify differential gene expression.
- Evaluated stromal remodeling via histological staining (H&E, Masson's Trichrome) in the BA-MaPS model.
Main Results:
- ERK5 deletion significantly impaired TNBC cell migration across all tested models.
- ERK5 inhibition altered transcriptomic profiles, affecting genes related to epithelial-to-mesenchymal transition (EMT), migration, and the matrisome.
- Histological analysis showed reduced collagen deposition with ERK5 depletion in the BA-MaPS model; NFκB pathway upregulation was model-dependent.
Conclusions:
- ERK5 is linked to TNBC progression via regulation of tumor microenvironment remodeling, EMT, and cell motility.
- Findings highlight the importance of physiologically relevant models (3D spheroids, BA-MaPS) over 2D cultures for studying breast cancer.
- ERK5 represents a potential therapeutic target for TNBC, warranting further investigation.
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