1α, 25-Dihydroxyvitamin D regulates hypoxia-inducible factor-1α in untransformed and Harvey-ras transfected breast epithelial cells.
1α, 25-Dihydroxyvitamin D regulates hypoxia-inducible factor-1α in untransformed and Harvey-ras transfected breast epithelial cells.
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DOI：
10.1016/j.canlet.2010.06.014
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发表时间：
2010-12-08
期刊：
影响因子：
9.7
通讯作者：
Teegarden, Dorothy
中科院分区：
文献类型：
--
作者：
Jiang, Yan;Zheng, Wei;Teegarden, Dorothy
The purpose of this study was to determine the mechanism by which 1α, 25-dihydroxyvitamin D (1,25(OH)2D) alters hypoxia inducible factor-1α (HIF-1α) protein in untransformed and Harvey-ras (H-ras) oncogene transfected MCF10A breast epithelial cells. Treatment with1,25(OH)2D (10 nM) increased both mRNA (2.55±0.6 fold vs. vehicle, p=0.03) and protein levels (2.37±0.3 fold vs. vehicle, p<0.0001) of HIF-1α in MCF10A cells in 12 hours, which remained elevated at 24 hours. However, in H-ras transfected MCF10A cells, 1,25(OH)2D treatment increased HIF-1α protein level (2.08±0.38 fold vs. vehicle, p= 0.05) at 12 hrs, with no change in mRNA level and HIF-1α protein level returned to baseline after 24 hours. A transcription inhibitor prevented the 1,25(OH)2D induction of HIF-1α protein and mRNA levels in MCF10A cells, but failed to alter the induction of HIF-1α protein level in H-ras transfected MCF10A cells. On the other hand, inhibition of proteasomal degradation prevented the 1,25(OH)2D-induced HIF-1α protein level in H-ras transfected MCF10A but not in MCF10A cells. These results support that 1,25(OH)2D regulates HIF-1α protein level via transcriptional regulation in MCF10A cells in contrast to through proteosomal degradation with the presence of H-ras oncogene in MCF10A cells.
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影响因子：
15.9
作者：
Solomon, C;White, JH;Kremer, R
通讯作者：
Kremer, R
影响因子：
11.5
作者：
Giatromanolaki, A;Koukourakis, MI;Sivridis, E
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作者：
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10.1006/bbrc.2001.5532
发表时间：
2001-09-14
影响因子：
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作者：
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通讯作者：
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影响因子：
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作者：
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通讯作者：
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