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Regulation of a rat VL30 element in human breast cancer cells in hypoxia and anoxia: role of HIF-1.

Ameri K, Burke B, Lewis CE, Harris AL - Br. J. Cancer (2002)

Bottom Line: Novel approaches to cancer gene therapy currently exploit tumour hypoxia to achieve transcriptional targeting using oxygen-regulated enhancer elements called hypoxia response elements.Mutational analysis demonstrated that the base immediately 5' to this modulates the anoxic/hypoxic induction of the secondary anoxia response element, such that TACGTG>GACGTG>CACGTG.A similar correlation was found for erythropoietin, phosphoglycerate kinase 1, and aldolase hypoxia response elements, which contain these respective 5' flanking bases.

View Article: PubMed Central - PubMed

Affiliation: Tumour Targeting Group, Division of Genomic Medicine, University of Sheffield Medical School, Beech Hill Road, Sheffield S10 2RX, UK.

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Related in: MedlinePlus

Mean (±s.e.m.) standardised LUC light units (ratio of firefly LUC/Renilla LUC readings) in either wild type (HIF-1 +/+) or HIF-1α knockout (HIF-1 −/−) CHO cells (Wood et al, 1998) following transfection with a pGL3 Promoter plasmid expressing firefly LUC under control of a trimer of the SARE, following exposure to 21% O2, 0.5% O2, or 0% O2 for 16 h. The SARE inducibility is lost in the HIF-1α knockout (HIF-1 −/−) CHO cells. P=0.003 with respect to HIF-1 +/+ cells at 21% O2, or the same oxygen tensions for HIF−/− cells.
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fig8: Mean (±s.e.m.) standardised LUC light units (ratio of firefly LUC/Renilla LUC readings) in either wild type (HIF-1 +/+) or HIF-1α knockout (HIF-1 −/−) CHO cells (Wood et al, 1998) following transfection with a pGL3 Promoter plasmid expressing firefly LUC under control of a trimer of the SARE, following exposure to 21% O2, 0.5% O2, or 0% O2 for 16 h. The SARE inducibility is lost in the HIF-1α knockout (HIF-1 −/−) CHO cells. P=0.003 with respect to HIF-1 +/+ cells at 21% O2, or the same oxygen tensions for HIF−/− cells.

Mentions: In wild type CHO cells, the SARE was induced in both anoxia and 0.5% O2. However, no SARE induction was observed in anoxia or 0.5% O2 in HIF knockout CHO cells (Figure 8Figure 8


Regulation of a rat VL30 element in human breast cancer cells in hypoxia and anoxia: role of HIF-1.

Ameri K, Burke B, Lewis CE, Harris AL - Br. J. Cancer (2002)

Mean (±s.e.m.) standardised LUC light units (ratio of firefly LUC/Renilla LUC readings) in either wild type (HIF-1 +/+) or HIF-1α knockout (HIF-1 −/−) CHO cells (Wood et al, 1998) following transfection with a pGL3 Promoter plasmid expressing firefly LUC under control of a trimer of the SARE, following exposure to 21% O2, 0.5% O2, or 0% O2 for 16 h. The SARE inducibility is lost in the HIF-1α knockout (HIF-1 −/−) CHO cells. P=0.003 with respect to HIF-1 +/+ cells at 21% O2, or the same oxygen tensions for HIF−/− cells.
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Related In: Results  -  Collection

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fig8: Mean (±s.e.m.) standardised LUC light units (ratio of firefly LUC/Renilla LUC readings) in either wild type (HIF-1 +/+) or HIF-1α knockout (HIF-1 −/−) CHO cells (Wood et al, 1998) following transfection with a pGL3 Promoter plasmid expressing firefly LUC under control of a trimer of the SARE, following exposure to 21% O2, 0.5% O2, or 0% O2 for 16 h. The SARE inducibility is lost in the HIF-1α knockout (HIF-1 −/−) CHO cells. P=0.003 with respect to HIF-1 +/+ cells at 21% O2, or the same oxygen tensions for HIF−/− cells.
Mentions: In wild type CHO cells, the SARE was induced in both anoxia and 0.5% O2. However, no SARE induction was observed in anoxia or 0.5% O2 in HIF knockout CHO cells (Figure 8Figure 8

Bottom Line: Novel approaches to cancer gene therapy currently exploit tumour hypoxia to achieve transcriptional targeting using oxygen-regulated enhancer elements called hypoxia response elements.Mutational analysis demonstrated that the base immediately 5' to this modulates the anoxic/hypoxic induction of the secondary anoxia response element, such that TACGTG>GACGTG>CACGTG.A similar correlation was found for erythropoietin, phosphoglycerate kinase 1, and aldolase hypoxia response elements, which contain these respective 5' flanking bases.

View Article: PubMed Central - PubMed

Affiliation: Tumour Targeting Group, Division of Genomic Medicine, University of Sheffield Medical School, Beech Hill Road, Sheffield S10 2RX, UK.

Show MeSH
Related in: MedlinePlus