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HIF-1 is induced via EGFR activation and mediates resistance to anoikis-like cell death under lipid rafts/caveolae-disrupting stress

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dc.contributor.authorLee, Seong-Hee-
dc.contributor.authorKoo, Kyung Hee-
dc.contributor.authorPark, Jong-Wan-
dc.contributor.authorKim, Hee-Jung-
dc.contributor.authorPark, Jong Bae-
dc.contributor.authorKim, Yong-Nyun-
dc.contributor.authorPark, Byung-Kiu-
dc.contributor.authorYe, Sang-Kyu-
dc.date.accessioned2012-07-02T05:54:40Z-
dc.date.available2012-07-02T05:54:40Z-
dc.date.issued2009-09-
dc.identifier.citationCARCINOGENESIS; Vol.30 12; 1997-2004ko_KR
dc.identifier.issn0143-3334-
dc.identifier.urihttps://hdl.handle.net/10371/78090-
dc.description.abstractThe plasma membrane microdomains, lipid rafts, are involved in regulation of cellular functions such as cell survival and adhesion. Cholesterol is a critical component of lipid rafts in terms of their integrity and functions and rafts disruption by cholesterol depletion can induce detachment-induced cell death. Hypoxia inducible factor-1 (HIF-1) alpha is stabilized in hypoxia and transactivates numerous genes required for cellular adaptation to hypoxia. It is also induced by non-hypoxic stimuli and contributes to cell survival. Because hypoxia inhibits cholesterol synthesis and HIF-1 alpha plays a role in this process, we here explored a possible connection between lipid rafts and HIF-1 alpha. We investigated whether HIF-1 alpha is regulated during cholesterol depletion/rafts disruption in A431 cells in normoxic conditions. Methyl-beta cyclodextrin (M beta CD), which induces cholesterol depletion, upregulated HIF-1 alpha even under normoxic conditions and this upregulation required epidermal growth factor receptor (EGFR) and extracellular signal-regulated kinase 1 and 2 activation, but not Akt activation. M beta CD treatment induced HIF-1 alpha upregulation at both the transcriptional and translational levels but not at the posttranslational levels. In addition, M beta CD robustly induced vascular endothelial growth factor production and stimulated an hypoxia response element-driven luciferase reporter activity under normoxic conditions, indicating that M beta CD-induced HIF-1 alpha is functionally activated. Both EGFR activity and HIF-1 alpha expression were higher in the attached cells than in the detached cells after M beta CD treatment. Furthermore, inhibition of HIF-1 alpha by RNA interference accelerated cell detachment, thus increasing cell death, indicating that HIF-1 alpha expression attenuates M beta CD-induced anoikis-like cell death. These data suggest that, depending on cholesterol levels, lipid rafts or membrane fluidity are probably to regulate HIF-1 alpha expression in normoxia by modulating rafts protein activities such as EGFR, and this connection between lipid rafts and HIF-1 alpha regulation may provide cell survival under membrane-disturbing stress.ko_KR
dc.language.isoenko_KR
dc.publisherOXFORD UNIV PRESSko_KR
dc.titleHIF-1 is induced via EGFR activation and mediates resistance to anoikis-like cell death under lipid rafts/caveolae-disrupting stressko_KR
dc.typeArticleko_KR
dc.contributor.AlternativeAuthor이성희-
dc.contributor.AlternativeAuthor구경희-
dc.contributor.AlternativeAuthor박종완-
dc.contributor.AlternativeAuthor김희중-
dc.contributor.AlternativeAuthor예상규-
dc.contributor.AlternativeAuthor박종배-
dc.contributor.AlternativeAuthor박병규-
dc.contributor.AlternativeAuthor김용년-
dc.identifier.doi10.1093/carcin/bgp233-
dc.citation.journaltitleCARCINOGENESIS-
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dc.description.tc4-
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