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Anticancer effect of rapamycin on MCF-7 via downregulation of VEGF expression
Takaaki Fujii1, Reina Yajima2, Hironori Tatsuki2
1Department of General Surgical Science, Graduate School of Medicine, Gunma University, 3-39-22 Showa-machi, Maebashi, Gunma, 371-8511, Japan. ftakaaki@gunma-u.ac.jp.
Abstract:
The importance of mTOR signaling in tumor biology is widely accepted and a number of agents that selectively target mTOR are being developed in cancer therapy. On the other hand, it has been demonstrated that mTOR can act as an angiogenic agent. Thus, we hypothesized that the mTOR inhibitor-induced anticancer effect is affected by expression of a key angiogenic factor, vascular endothelial growth factor (VEGF) and investigated the anticancer effect underlying mTOR using an in vitro assay. The mTOR inhibitor rapamycin dose-dependently reduced the cell viability of the breast cancer cell line, MCF-7, but did not reduce the cell viability of the colon cancer cell line, HT-29. Rapamycin reduced the VEGF expression in the culture medium of MCF-7, while rapamycin did not contribute VEGF expression in the culture medium of HT-29. VEGF stimulated cell viability and VEGF inhibition reduced cell viability of MCF-7, and rapamycin dose-dependently restored the cell viability of MCF-7 reduced by rapamycin. These findings suggest that mTOR acts as a direct anticancer agent and that the mTOR-inhibitor-induced anticancer effect involved the reduced expression of VEGF in MCF-7. Our results imply that mTOR regulates the expression of VEGF and is involved in breast cancer progression.
Insights
mTOR inhibition reduced breast cancer cell viability by decreasing vascular endothelial growth factor (VEGF) expression. This suggests mTOR is an anticancer target, regulating VEGF and impacting breast cancer progression.
Area of Science:
- Molecular Biology
- Oncology
- Cancer Research
Background:
- Mammalian target of rapamycin (mTOR) signaling is crucial in tumor biology, with mTOR inhibitors being developed for cancer therapy.
- mTOR has been shown to function as an angiogenic agent, suggesting a complex role in cancer progression.
Purpose of the Study:
- To investigate the anticancer effects of mTOR inhibition in vitro.
- To determine if the mTOR inhibitor-induced anticancer effect is influenced by vascular endothelial growth factor (VEGF) expression.
Main Methods:
- Utilized an in vitro assay with breast cancer (MCF-7) and colon cancer (HT-29) cell lines.
- Administered the mTOR inhibitor rapamycin and measured cell viability and VEGF expression in culture medium.
- Assessed the impact of VEGF on cell viability and the restoration of cell viability by rapamycin.
Main Results:
- Rapamycin dose-dependently reduced MCF-7 cell viability but not HT-29 cell viability.
- Rapamycin decreased VEGF expression in MCF-7 cultures, but not in HT-29 cultures.
- VEGF stimulation increased MCF-7 cell viability, while VEGF inhibition reduced it; rapamycin restored viability.
Conclusions:
- mTOR acts as a direct anticancer agent, and its inhibitor-induced effect involves reduced VEGF expression in MCF-7 cells.
- mTOR regulates VEGF expression, indicating its involvement in breast cancer progression.
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