Journal
CELL REPORTS
Volume 17, Issue 6, Pages 1621-1631Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2016.10.020
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Funding
- Japan Society for the Promotion of Science (JSPS) Postdoctoral Fellowships for Research Abroad [H25-480]
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Ovarian Cancer Research Fund Alliance
- Foundation for Women's Cancer
- Colleen's Dream Foundation
- Cancer Prevention and Research Institute of Texas (CPRIT) [RP101502, RP101489]
- Computational Cancer Biology Training Program from CPRIT [RP140113]
- Caring Together
- NY Ovarian Cancer Research Grant from the Foundation for Women's Cancer
- National Cancer Institute (NCI) the National Cancer Institute's Clinical Proteomic Tumor Analysis Consortium (CPTAC) program [U24CA160019, U54 CA096300]
- NIH [CA016672, P50 CA083639, P50 CA098258, U54 CA151668, UH3 TR000943]
- CPRIT [RP110595, DP 150091]
- American Cancer Society Research Professor Award
- Blanton Davis Ovarian Cancer Research Program
- RGK Foundation
- Frank McGraw Memorial Chair in Cancer Research
- John S. Dunn Foundation
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Even though hyperthermia is a promising treatment for cancer, the relationship between specific temperatures and clinical benefits and predictors of sensitivity of cancer to hyperthermia is poorly understood. Ovarian and uterine tumors have diverse hyperthermia sensitivities. Integrative analyses of the specific gene signatures and the differences in response to hyperthermia between hyperthermia-sensitive and -resistant cancer cells identified CTGF as a key regulator of sensitivity. CTGF silencing sensitized resistant cells to hyperthermia. CTGF small interfering RNA (siRNA) treatment also sensitized resistant cancers to localized hyperthermia induced by copper sulfide nanoparticles and near-infrared laser in orthotopic ovarian cancer models. CTGF silencing aggravated energy stress induced by hyperthermia and enhanced apoptosis of hyperthermia-resistant cancers.
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