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Updated: Mar 27, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020
Serum deprivation response inhibits breast cancer progression by blocking transforming growth factor-β signaling
Yao Tian1,2,3, Yue Yu1,2,3, Li-Kun Hou1,2,3
1The First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, China.
Abstract:
Serum deprivation response (SDPR), a key substrate for protein kinase C, play a critical role in inducing membrane curvature and participate in the formation of caveolae. However, the function of SDPR in cancer development and progression is still not clear. Here, we found that SDPR is downregulated in human breast cancer. Overexpression of SDPR suppresses cell proliferation and invasion in MDA-MB-231 cells, while depletion of SDPR promotes cell proliferation and invasion in MCF10A cells. Subsequently, SDPR depletion induces epithelial-mesenchymal transition (EMT)-like phenotype. Finally, knockdown of SDPR activates transforming growth factor-β (TGF-β) signaling by upregulation of TGF-β1 expression. In conclusion, our results showed that SDPR inhibits breast cancer progression by blocking TGF-β signaling. Serum deprivation response suppresses cell proliferation and invasion in breast cancer cells. SDPR depletion induces epithelial-mesenchymal transition by activation of TGF-β signaling.
Insights
Serum deprivation response (SDPR) inhibits breast cancer progression by suppressing cell proliferation and invasion. SDPR downregulation activates transforming growth factor-β (TGF-β) signaling, promoting epithelial-mesenchymal transition and cancer advancement.
Area of Science:
- Molecular Biology
- Cancer Research
- Cell Biology
Background:
- Serum deprivation response (SDPR) is involved in membrane dynamics and caveolae formation.
- The role of SDPR in cancer, particularly breast cancer, remains largely undefined.
Purpose of the Study:
- To investigate the function of SDPR in breast cancer development and progression.
- To elucidate the molecular mechanisms underlying SDPR's role in cancer.
Main Methods:
- Analysis of SDPR expression in human breast cancer tissues.
- Overexpression and depletion studies in breast cancer cell lines (MDA-MB-231) and normal breast epithelial cells (MCF10A).
- Assessment of cell proliferation, invasion, epithelial-mesenchymal transition (EMT) markers, and transforming growth factor-β (TGF-β) signaling pathway activation.
Main Results:
- SDPR expression is downregulated in human breast cancer.
- Overexpression of SDPR inhibited proliferation and invasion in MDA-MB-231 cells.
- Depletion of SDPR promoted proliferation and invasion in MCF10A cells, inducing an EMT-like phenotype.
- SDPR depletion led to the activation of TGF-β signaling via upregulation of TGF-β1.
Conclusions:
- SDPR acts as a tumor suppressor in breast cancer.
- SDPR inhibits breast cancer progression by suppressing cell proliferation and invasion.
- SDPR blocks TGF-β signaling, thereby preventing EMT and cancer advancement.
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