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Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
Published on: March 20, 2020
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MFAP5 promotes basal-like breast cancer progression by activating the EMT program
Yanmei Wu1, Ping Wu2, Quan Zhang1
11Department of Breast Surgery, Changhai Hospital, Naval Medical University, 800 Xiangyin Road, Shanghai, 200433 China.
Cell & Bioscience
|March 23, 2019
Summary
Microfibrillar-associated protein 5 (MFAP5) drives aggressive basal-like breast cancer (BLBC) growth and metastasis. Inhibiting TGF-β/Notch pathways may offer therapeutic strategies for this challenging malignancy.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Basal-like breast cancer (BLBC) is aggressive with poor prognosis and limited treatment options.
- Microfibrillar-associated protein 5 (MFAP5) is overexpressed in BLBC and linked to reduced survival.
- The precise role of MFAP5 in BLBC progression requires further elucidation.
Purpose of the Study:
- To investigate the functional role of MFAP5 in human basal-like breast cancer.
- To identify potential therapeutic targets for BLBC based on MFAP5 function.
Main Methods:
- In vitro and in vivo functional analyses were performed to assess MFAP5's role.
- Animal models were utilized to study MFAP5's impact on BLBC proliferation and metastasis.
- The effects of TGF-β and Notch pathway inhibitors were evaluated.
Main Results:
- MFAP5 overexpression significantly enhanced BLBC proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) markers.
- MFAP5 promoted BLBC proliferation and metastasis in vivo, confirmed by animal models.
- Inhibitors of the TGF-β or Notch pathways reversed MFAP5-induced tumorigenicity and metastasis.
Conclusions:
- MFAP5 promotes EMT in BLBC metastasis.
- The TGF-β/Notch pathway is implicated in MFAP5-driven BLBC metastasis.
- Targeting the TGF-β/Notch pathway may be a viable strategy for treating MFAP5-driven BLBC.
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