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pubmed-article:19956670pubmed:abstractTextHypoxia-mediated HIF-1alpha stabilization and NF-kappaB activation play a key role in carcinogenesis by fostering cancer cell survival, angiogenesis and tumor invasion. Gangliosides are integral components of biological membranes with an increasingly recognized role as signaling intermediates. In particular, ganglioside GD3 has been characterized as a proapoptotic lipid effector by promoting cell death signaling and suppression of survival pathways. Thus, our aim was to analyze the role of GD3 in hypoxia susceptibility of hepatocarcinoma cells and in vivo tumor growth.lld:pubmed
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pubmed-article:19956670pubmed:authorpubmed-author:EnrichCarlosClld:pubmed
pubmed-article:19956670pubmed:authorpubmed-author:MoralesAlbert...lld:pubmed
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pubmed-article:19956670pubmed:authorpubmed-author:LluisJosep...lld:pubmed
pubmed-article:19956670pubmed:authorpubmed-author:Fernandez-Che...lld:pubmed
pubmed-article:19956670pubmed:authorpubmed-author:LlacunaLauraLlld:pubmed
pubmed-article:19956670pubmed:authorpubmed-author:BárcenaCristi...lld:pubmed
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pubmed-article:19956670pubmed:articleTitleGD3 synthase overexpression sensitizes hepatocarcinoma cells to hypoxia and reduces tumor growth by suppressing the cSrc/NF-kappaB survival pathway.lld:pubmed
pubmed-article:19956670pubmed:affiliationDepartment of Cell Death and Proliferation, IIBB-CSIC, and Liver Unit, Hospital Clinic, IDIBAPS-CIBEK, CIBEREHD, Barcelona, Spain.lld:pubmed
pubmed-article:19956670pubmed:publicationTypeJournal Articlelld:pubmed
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