Oestrogen Represses Noggin Expression by Interfering With BMP/Smad Signalling in ER Positive Breast Cancer
Ming Liu1,2, Debby Koo1, Wen G Jiang1
1Cardiff China Medical Research Collaborative, Division of Cancer & Genetics, Cardiff University School of Medicine, Cardiff, U.K.
Anticancer Research
|July 26, 2024
Summary
Noggin protein promotes breast cancer cell growth and resistance to therapies like tamoxifen. Oestrogen represses Noggin, suggesting a therapeutic target for oestrogen receptor-positive breast cancer.
Area of Science:
- Oncology
- Molecular Biology
- Endocrinology
Background:
- Noggin, a bone morphogenetic protein antagonist, is implicated in osteolytic bone metastases.
- Its specific role in oestrogen receptor (ER)-positive breast cancer warrants further investigation.
Purpose of the Study:
- To dissect the role of Noggin in ER-positive breast cancer.
- To investigate the regulation of Noggin by oestrogen and its impact on cellular functions and drug response.
Main Methods:
- Noggin expression was analyzed in ER-positive breast cancer cell lines (MCF-7, T-47D) under varying oestrogen conditions.
- BMP/Smad signaling activation and cellular functions were assessed.
- Drug responses to tamoxifen and chemotherapy were evaluated in Noggin-overexpressing cells.
Main Results:
- Noggin expression inversely correlated with ERα and was upregulated by oestrogen deprivation.
- Noggin overexpression increased MCF-7 and T-47D cell proliferation.
- Noggin-overexpressing cells showed enhanced tolerance to tamoxifen, DTX, and 5-FU.
Conclusions:
- Oestrogen represses Noggin expression via BMP/Smad signaling interference.
- Noggin overexpression promotes proliferation and contributes to drug resistance in ER-positive breast cancer cells.
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