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Updated: Jun 14, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020
ErbB/EGF signaling and EMT in mammary development and breast cancer
Katharine M Hardy1, Brian W Booth, Mary J C Hendrix
1Children's Memorial Research Center, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, 2300 Children's Plaza, Chicago, IL 60614, USA.
Abstract:
Activation of the ErbB family of receptor tyrosine kinases via cognate Epidermal Growth Factor (EGF)-like peptide ligands constitutes a major group of related signaling pathways that control proliferation, survival, angiogenesis and metastasis of breast cancer. In this respect, clinical trials with various ErbB receptor blocking antibodies and specific tyrosine kinase inhibitors have proven to be partially efficacious in the treatment of this heterogeneous disease. Induction of an embryonic program of epithelial-to-mesenchymal transition (EMT) in breast cancer, whereupon epithelial tumor cells convert to a more mesenchymal-like phenotype, facilitates the migration, intravasation, and extravasation of tumor cells during metastasis. Breast cancers which exhibit properties of EMT are highly aggressive and resistant to therapy. Activation of ErbB signaling can regulate EMT-associated invasion and migration in normal and malignant mammary epithelial cells, as well as modulating discrete stages of mammary gland development. The purpose of this review is to summarize current information regarding the role of ErbB signaling in aspects of EMT that influence epithelial cell plasticity during mammary gland development and tumorigenesis. How this information may contribute to the improvement of therapeutic approaches in breast cancer will also be addressed.
Insights
ErbB signaling pathways drive breast cancer growth and metastasis by promoting epithelial-to-mesenchymal transition (EMT). Understanding ErbB
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- ErbB receptor tyrosine kinases and Epidermal Growth Factor (EGF)-like ligands are crucial in breast cancer proliferation, survival, angiogenesis, and metastasis.
- ErbB signaling pathways are implicated in regulating epithelial-to-mesenchymal transition (EMT), a process linked to aggressive, therapy-resistant breast cancers.
- Current therapies targeting ErbB receptors show partial efficacy in treating heterogeneous breast cancer.
Purpose of the Study:
- To review the role of ErbB signaling in epithelial cell plasticity during mammary gland development and tumorigenesis, focusing on EMT.
- To explore how ErbB-mediated EMT influences breast cancer progression and metastasis.
- To discuss the potential of this knowledge in improving therapeutic strategies for breast cancer.
Main Methods:
- Literature review of current scientific information on ErbB signaling, EMT, and breast cancer.
- Analysis of the interplay between ErbB pathways and EMT in normal mammary gland development and cancer.
- Synthesis of findings to inform potential therapeutic advancements.
Main Results:
- ErbB signaling activation is a key driver of EMT, enhancing tumor cell migration, invasion, and metastasis.
- EMT-associated breast cancers exhibit increased aggressiveness and therapeutic resistance.
- ErbB signaling influences EMT at various stages of mammary gland development and in tumorigenesis.
Conclusions:
- ErbB signaling plays a critical role in regulating EMT, impacting breast cancer progression and treatment outcomes.
- Targeting ErbB-mediated EMT pathways may offer novel therapeutic avenues for aggressive and resistant breast cancers.
- Further research into ErbB-EMT interactions is essential for developing more effective breast cancer therapies.
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