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Updated: Jul 2, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020
BCAR3 regulates EGF-induced DNA synthesis in normal human breast MCF-12A cells
Myung-Ju Oh1, Ton van Agthoven, Ji-Eun Choi
1Department of Nanomedical Engineering, Pusan National University, Miryang, Geongnam 727-706, Republic of Korea.
Abstract:
BCAR3 (breast cancer anti-estrogen resistance 3) is a signal transducer containing an SH2 domain, a proline/serine-rich domain and a GDP-exchange factor homologous domain, whose role in signaling pathways is currently unclear. Furthermore, BCAR3 is implicated in anti-estrogen resistance of breast cancer cells. In the present study, we investigated the functional role of BCAR3 in a mitogenic signaling pathway of EGF in non-tumorigenic human breast epithelial MCF-12A cells. Microinjection of an anti-BCAR3 antibody, siRNAs targeting BCAR3 and an SH2 domain of BCAR3 inhibited EGF-induced DNA synthesis. Direct association of BCAR3 with activated EGF receptor and Cas was observed. Lastly, microinjection of a BCAR3 expression plasmid induced DNA synthesis. These findings suggest that the BCAR3 protein, through its SH2 domain, is involved in the signaling pathways of EGF leading to cell cycle progression, and that BCAR3 itself is part of a mitogenic signaling pathway.
Insights
Breast cancer anti-estrogen resistance 3 (BCAR3) acts as a signal transducer in epidermal growth factor (EGF) pathways. This study reveals BCAR3
Area of Science:
- Cell Biology
- Molecular Biology
- Oncology
Background:
- BCAR3 (breast cancer anti-estrogen resistance 3) is a signal transducer with unclear roles in cellular signaling.
- BCAR3 is associated with anti-estrogen resistance in breast cancer cells.
- Understanding BCAR3's function is crucial for breast cancer research.
Purpose of the Study:
- To investigate the functional role of BCAR3 in the mitogenic signaling pathway of EGF.
- To elucidate BCAR3's involvement in EGF-induced cell cycle progression.
- To determine if BCAR3 is part of a mitogenic signaling pathway.
Main Methods:
- Utilized microinjection of anti-BCAR3 antibody and BCAR3-targeting siRNAs in MCF-12A cells.
- Investigated direct association of BCAR3 with activated EGF receptor and Cas.
- Employed microinjection of a BCAR3 expression plasmid to assess its effects.
Main Results:
- Inhibition of EGF-induced DNA synthesis upon BCAR3 antibody or siRNA microinjection.
- Demonstrated direct association between BCAR3, activated EGF receptor, and Cas.
- Induced DNA synthesis following microinjection of a BCAR3 expression plasmid.
Conclusions:
- BCAR3, via its SH2 domain, participates in EGF signaling pathways that drive cell cycle progression.
- BCAR3 is identified as a component of a mitogenic signaling pathway.
- Findings suggest BCAR3's potential role in regulating cell proliferation.
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