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Article: Hypoxia-inducible factor-1-mediated activation of stanniocalcin-1 in human cancer cells

TitleHypoxia-inducible factor-1-mediated activation of stanniocalcin-1 in human cancer cells
Authors
Issue Date2005
PublisherThe Endocrine Society. The Journal's web site is located at http://endo.endojournals.org
Citation
Endocrinology, 2005, v. 146 n. 11, p. 4951-4960 How to Cite?
AbstractStanniocalcin-1 (STC1) is an endocrine hormone originally discovered in the corpuscles of Stannius, endocrine glands on kidneys of bony fishes, and also has been identified in mammals. The mammalian STC1 gene is widely expressed in various tissues and appears to be involved in diverse biological processes. There is growing evidence to suggest that altered patterns of gene expression have a role in human cancer development. Recently STC1 has been identified as a stimulator of mitochondrial respiration and has been hypothesized to be functionally related to the Warburg effect, of which hypoxia-inducible factor (HIF)-1 plays a key role in reprogramming tumor metabolism. This prompted us to examine the involvement of HIF-1 in the regulation of STC1 expression in tumor hypoxia. Our data reveal that hypoxia can stimulate STC1 gene expression in various human cancer cell lines, including those derived from colon carcinomas, nasopharyngeal cancer (CNE-2, HONE-1, HK-1), and ovarian cancer (CaOV3, OVCAR3, SKOV3). By far, the greatest response was observed in CNE-2 cells. In further studies on CNE-2 cells, desferrioxamine, cobalt chloride, and O 2 depletion all increased HIF-1α protein and STC1 mRNA levels. Desferrioxamine treatment, when coupled with Fe replenishment, abolished these effects. RNA interference studies further confirmed that endogenous HIF-1α was a key factor in hypoxia-induced STC1 expression. The ability of vascular endothelial growth factor to stimulate STC1 expression in CNE-2 cells was comparatively low. Collectively, the present findings provide the first evidence of HIF-1 regulation of STC1 expression in human cancer cells. The studies have implications as to the role of STC1 in hypoxia induced adaptive responses in tumor cells. Copyright © 2005 by The Endocrine Society.
Persistent Identifierhttp://hdl.handle.net/10722/183394
ISSN
2015 Impact Factor: 4.159
2015 SCImago Journal Rankings: 2.363
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYeung, HYen_US
dc.contributor.authorLai, KPen_US
dc.contributor.authorChan, HYen_US
dc.contributor.authorMak, NKen_US
dc.contributor.authorWagner, GFen_US
dc.contributor.authorWong, CKCen_US
dc.date.accessioned2013-05-27T07:12:31Z-
dc.date.available2013-05-27T07:12:31Z-
dc.date.issued2005en_US
dc.identifier.citationEndocrinology, 2005, v. 146 n. 11, p. 4951-4960en_US
dc.identifier.issn0013-7227en_US
dc.identifier.urihttp://hdl.handle.net/10722/183394-
dc.description.abstractStanniocalcin-1 (STC1) is an endocrine hormone originally discovered in the corpuscles of Stannius, endocrine glands on kidneys of bony fishes, and also has been identified in mammals. The mammalian STC1 gene is widely expressed in various tissues and appears to be involved in diverse biological processes. There is growing evidence to suggest that altered patterns of gene expression have a role in human cancer development. Recently STC1 has been identified as a stimulator of mitochondrial respiration and has been hypothesized to be functionally related to the Warburg effect, of which hypoxia-inducible factor (HIF)-1 plays a key role in reprogramming tumor metabolism. This prompted us to examine the involvement of HIF-1 in the regulation of STC1 expression in tumor hypoxia. Our data reveal that hypoxia can stimulate STC1 gene expression in various human cancer cell lines, including those derived from colon carcinomas, nasopharyngeal cancer (CNE-2, HONE-1, HK-1), and ovarian cancer (CaOV3, OVCAR3, SKOV3). By far, the greatest response was observed in CNE-2 cells. In further studies on CNE-2 cells, desferrioxamine, cobalt chloride, and O 2 depletion all increased HIF-1α protein and STC1 mRNA levels. Desferrioxamine treatment, when coupled with Fe replenishment, abolished these effects. RNA interference studies further confirmed that endogenous HIF-1α was a key factor in hypoxia-induced STC1 expression. The ability of vascular endothelial growth factor to stimulate STC1 expression in CNE-2 cells was comparatively low. Collectively, the present findings provide the first evidence of HIF-1 regulation of STC1 expression in human cancer cells. The studies have implications as to the role of STC1 in hypoxia induced adaptive responses in tumor cells. Copyright © 2005 by The Endocrine Society.en_US
dc.languageengen_US
dc.publisherThe Endocrine Society. The Journal's web site is located at http://endo.endojournals.orgen_US
dc.relation.ispartofEndocrinologyen_US
dc.subject.meshAnoxia - Chemically Induced - Metabolismen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshColonic Neoplasms - Metabolismen_US
dc.subject.meshDeferoxamine - Pharmacologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshFerric Compounds - Pharmacologyen_US
dc.subject.meshFerricyanides - Pharmacologyen_US
dc.subject.meshGlycoproteins - Antagonists & Inhibitors - Genetics - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshIron Chelating Agents - Pharmacologyen_US
dc.subject.meshNasopharyngeal Neoplasms - Metabolismen_US
dc.subject.meshNitric Oxide Donors - Pharmacologyen_US
dc.subject.meshNitroprusside - Pharmacologyen_US
dc.subject.meshOvarian Neoplasms - Metabolismen_US
dc.subject.meshRna, Messenger - Biosynthesisen_US
dc.subject.meshRna, Small Interferingen_US
dc.subject.meshTransfectionen_US
dc.titleHypoxia-inducible factor-1-mediated activation of stanniocalcin-1 in human cancer cellsen_US
dc.typeArticleen_US
dc.identifier.emailLai, KP: ballllai@hotmail.comen_US
dc.identifier.authorityLai, KP=rp01753en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1210/en.2005-0365en_US
dc.identifier.pmid16109785-
dc.identifier.scopuseid_2-s2.0-26844510900en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-26844510900&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume146en_US
dc.identifier.issue11en_US
dc.identifier.spage4951en_US
dc.identifier.epage4960en_US
dc.identifier.isiWOS:000232585200043-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridYeung, HY=7102212132en_US
dc.identifier.scopusauthoridLai, KP=7402135707en_US
dc.identifier.scopusauthoridChan, HY=55464804900en_US
dc.identifier.scopusauthoridMak, NK=35587830100en_US
dc.identifier.scopusauthoridWagner, GF=7404372679en_US
dc.identifier.scopusauthoridWong, CKC=35276549400en_US

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