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Hypoxia-induced radioresistance is independent of hypoxia-inducible factor-1A in vitro

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Title: Hypoxia-induced radioresistance is independent of hypoxia-inducible factor-1A in vitro
Authors: Arvold, Nils D.1, Guha, Neela2, Wang, Dongfang2, Matli, Mary2, Deen, Dennis F.1,3, Warren, Robert S.2 warrenr@surgery.ucsf.edu, Haas-Kogan, Daphne A.1,3
Source: International Journal of Radiation Oncology, Biology, Physics. May2005, Vol. 62 Issue 1, p207-212. 6p.
Subjects: Cerebral anoxia, Hypoxemia, Cell lines, Transcription factors
Abstract: Purpose: We sought to determine whether hypoxia-induced radioresistance is mediated by the transcription factor hypoxia-inducible factor-1a (HIF-1a). Methods and materials: We used 2 mouse embryonic fibroblast cell lines transformed with H-ras and TAg, 1 HIF-1a+/+ and the other HIF-1a-/-. Cell were exposed to either 95% air and 5% CO2 (normoxic conditions) or 0.2% O2, 94.8% N2, and 5% CO2 (hypoxic conditions) for 4 hours. Cells were then irradiated and subjected to clonogenic survival assays. Results: Whereas neither +/+ ras/TAg nor -/- ras/TAg cells expressed HIF-1a under normoxic conditions, hypoxia induced expression of HIF-1a only in +/+ ras/TAg cells, confirming the absence of HIF-1a in -/- ras/TAg cells. Clonogenic survival curves for +/+ ras/TAg and -/- ras/TAg cells under normoxia and hypoxia demonstrated that hypoxia increased radioresistance in both cell lines to the same degree. At 1-log cell kill, the +/+ ras/TAg and -/- ras/TAg cells had an identical oxygen enhancement ratio of 1.28 ± 0.09 and nearly identical oxygen enhancement ratios at 2-log cell kill. Conclusion: In our system of transformed mouse embryonic fibroblasts, hypoxia-mediated radiation resistance is independent of HIF-1a. [Copyright &y& Elsevier]
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Database: Engineering Source
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Abstract:Purpose: We sought to determine whether hypoxia-induced radioresistance is mediated by the transcription factor hypoxia-inducible factor-1a (HIF-1a). Methods and materials: We used 2 mouse embryonic fibroblast cell lines transformed with H-ras and TAg, 1 HIF-1a+/+ and the other HIF-1a-/-. Cell were exposed to either 95% air and 5% CO2 (normoxic conditions) or 0.2% O2, 94.8% N2, and 5% CO2 (hypoxic conditions) for 4 hours. Cells were then irradiated and subjected to clonogenic survival assays. Results: Whereas neither +/+ ras/TAg nor -/- ras/TAg cells expressed HIF-1a under normoxic conditions, hypoxia induced expression of HIF-1a only in +/+ ras/TAg cells, confirming the absence of HIF-1a in -/- ras/TAg cells. Clonogenic survival curves for +/+ ras/TAg and -/- ras/TAg cells under normoxia and hypoxia demonstrated that hypoxia increased radioresistance in both cell lines to the same degree. At 1-log cell kill, the +/+ ras/TAg and -/- ras/TAg cells had an identical oxygen enhancement ratio of 1.28 ± 0.09 and nearly identical oxygen enhancement ratios at 2-log cell kill. Conclusion: In our system of transformed mouse embryonic fibroblasts, hypoxia-mediated radiation resistance is independent of HIF-1a. [Copyright &y& Elsevier]
ISSN:03603016
DOI:10.1016/j.ijrobp.2005.01.019