Inhibition of mTOR radiosensitizes soft tissue sarcoma and tumor vasculature
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Abstract
PURPOSE: The PI3K/Akt/mTOR prosurvival pathway is frequently up-regulated in soft tissue sarcoma. Mammalian target of rapamycin (mTOR) inhibitors, such as rapamycin, have recently shown clinical benefit in soft tissue sarcoma, and mTOR inhibition has also been associated with radiosensitization of carcinoma and endothelial cells. This study tested the hypothesis that rapamycin radiosensitizes soft tissue sarcoma and endothelial cells in vitro and in vivo through the inhibition of mTOR. EXPERIMENTAL DESIGN: Colony formation assays were done to determine the radiosensitizing properties of rapamycin on three human soft tissue sarcoma cell lines (SK-LMS-1, SW-872, and HT-1080) and human dermal microvascular endothelial cells (HDMEC). The functional effects of rapamycin and radiation on the endothelial compartment were evaluated with microvascular sprouting assays. The in vivo radiosensitizing activity of rapamycin was assessed with s.c. SK-LMS-1 nude mice xenografts treated with concurrent daily rapamycin, radiation, or both for three weeks. RESULTS: In vitro radiosensitization was shown in all three soft tissue sarcoma cell lines with minimally cytotoxic doses of rapamycin. SK-LMS-1 xenografts displayed significant tumor growth delay with rapamycin and radiation compared with either treatment alone. Radiation resulted in transient increased mTOR function, whereas rapamycin abolished this signaling in irradiated and unirradiated samples. In HDMEC, rapamycin and radiation reduced microvessel sprouting, but did not alter colony formation. CONCLUSIONS: Minimally cytotoxic concentrations of rapamycin inhibited the mTOR cascade in culture and in vivo while radiosensitizing soft tissue sarcoma, and produced synergistic effects with radiation on HDMEC microvessel formation. By targeting both tumor and endothelial compartments, rapamycin produced potent radiosensitization of soft tissue sarcoma xenografts. Clinical trials combining rapamycin and radiotherapy in soft tissue sarcoma are warranted.
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mTOR inhibitors can sensitize other tumor types to radiation.
“Given that mTOR inhibitors can sensitize other tumor types to radiation (Eshleman et al., 2002; Konstantinidou et al., 2009; Murphy et al., 2009)”
From mTOR inhibition prevents epithelial stem cell senescence and protects from radiation-induced mucositis (2012) · cites this paper as Murphy et al., 2009
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- Authors
- Murphy, J. D., Spalding, A. C., Somnay, Y. R., Markwart, S., Ray, M. E., & Hamstra, D. A.
- Affiliations
- University of Michigan (US)
- Venue
- Clinical Cancer Research
- Published
- 2009-01-15
- Volume
- 15
- Issue
- 2
- Pages
- 589-596
- ISSN
- 1078-0432 (ISSN-L)
- 1557-3265
- OpenAlex
- W2101308683
- Cited by
- 44
- References
- 50
- Citations by year
- 2025: 1 · 2022: 2 · 2021: 2 · 2020: 2 · 2017: 3 · 2016: 2 · 2015: 3 · 2014: 2 · 2013: 3 · 2012: 4
- FWCI
- 3.21
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Clinical Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Sarcoma Diagnosis and Treatment
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Keywords
- mTOR inhibition, rapamycin, soft tissue sarcoma, radiosensitization, PI3K/AKT/mTOR pathway, tumor vasculature, endothelial cells, microvessel sprouting, radiotherapy, combination therapy, tumor xenografts
- MeSH terms
- Animals, Antineoplastic Agents, Carcinoma, Dose-Response Relationship, Radiation, Endothelium, Humans, Mice, Nude, Microcirculation, Models, Biological, Neoplasm Transplantation, Protein Kinases, Radiation-Sensitizing Agents, Sarcoma, Sirolimus, Endothelial Cells, Cell Line, Tumor, Mice, TOR Serine-Threonine Kinases
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