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Updated: Feb 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
Rapamycin enhances the antiproliferative effect of transforming growth factor-β on MCF-7 human breast cancer cells
1Department of Oncology, Cancer Center, West China Hospital, Sichuan University and Collaborative Innovation Center of Biotherapy, Chengdu, Sichuan 610041, P.R. China.
Abstract:
Transforming growth factor-β (TGF-β), a well-known cytokine with pleiotropic biological functions, has an important role in the regulation of cellular proliferation. Rapamycin has specific antagonistic activity on the function of the mammalian target of the rapamycin signaling pathway. The cooperation of TGF-β and rapamycin on the proliferation of Michigan Cancer Foundation (MCF)-7 human breast cancer cells is unclear. The present study demonstrated that TGF-β had a growth-arresting effect on MCF-7 cancer cells. TGF-β stimulation resulted in the upregulation of several cyclin-dependent kinase inhibitors, including p14ARF, p15INK4b, p16INK4a and p21WAF1/CIP1. The present study also demonstrated that rapamycin enhances the antiproliferative effect of TGF-β. The combination of rapamycin and TGF-β induced apoptosis of MCF-7 tumor cells. These findings advance the current understanding of the biological effects of TGF-β and rapamycin.
Insights
Transforming growth factor-β (TGF-β) inhibits breast cancer cell proliferation by upregulating cyclin-dependent kinase inhibitors. Rapamycin enhances this effect, leading to apoptosis in MCF-7 cells.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Transforming growth factor-β (TGF-β) is a cytokine regulating cellular proliferation.
- Rapamycin targets the mammalian target of the rapamycin (mTOR) signaling pathway.
- The combined effect of TGF-β and rapamycin on MCF-7 human breast cancer cells is not well understood.
Purpose of the Study:
- To investigate the synergistic effects of TGF-β and rapamycin on MCF-7 human breast cancer cell proliferation.
- To elucidate the molecular mechanisms underlying the interaction between TGF-β and rapamycin in breast cancer cells.
Main Methods:
- MCF-7 human breast cancer cells were treated with TGF-β and/or rapamycin.
- Cell proliferation was assessed.
- Expression levels of cyclin-dependent kinase inhibitors (p14ARF, p15INK4b, p16INK4a, p21WAF1/CIP1) were analyzed.
- Apoptosis was evaluated.
Main Results:
- TGF-β demonstrated a significant growth-arresting effect on MCF-7 cells.
- TGF-β stimulation led to increased expression of p14ARF, p15INK4b, p16INK4a, and p21WAF1/CIP1.
- Rapamycin potentiated the antiproliferative action of TGF-β.
- The combination of rapamycin and TGF-β induced apoptosis in MCF-7 cells.
Conclusions:
- TGF-β exhibits antiproliferative effects on MCF-7 breast cancer cells, mediated by cyclin-dependent kinase inhibitors.
- Rapamycin enhances the antiproliferative and pro-apoptotic effects of TGF-β in these cells.
- The findings provide novel insights into the combined therapeutic potential of TGF-β and rapamycin in breast cancer treatment.
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