期刊
CANCER CELL
卷 8, 期 2, 页码 99-110出版社
CELL PRESS
DOI: 10.1016/j.ccr.2005.06.016
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资金
- NCI NIH HHS [CA40355] Funding Source: Medline
- NIBIB NIH HHS [EB00188-01] Funding Source: Medline
We have previously shown that radiation increases HIF-1 activity in tumors, causing significant radioprotection of the tumor vasculature. The impact that HIF-1 activation has on overall tumor radiosensitivity, however, is unknown. We reveal here that HIF-1 plays an important role in determining tumor radioresponsiveness through regulating four distinct processes. By promoting ATP metabolism, proliferation, and p53 activation, HIF-1 has a radiosensitizing effect on tumors. Through stimulating endothelial cell survival, HIF-1 promotes tumor radioresistance. As a result, the net effect of HIF-11 blockade on tumor radioresponsiveness is highly dependent on treatment sequencing, with radiation first strategies being significantly more effective than the alternative. These data provide a strong rationale for pursuing sequence-specific combinations of HIF-1 blockade and conventional therapeutics.
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