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dc.contributor.authorIrmak, M. B.en_US
dc.contributor.authorInce, G.en_US
dc.contributor.authorOzturk, M.en_US
dc.contributor.authorCetin Atalay, R.en_US
dc.date.accessioned2016-02-08T10:29:06Z
dc.date.available2016-02-08T10:29:06Z
dc.date.issued2003en_US
dc.identifier.issn0008-5472
dc.identifier.urihttp://hdl.handle.net/11693/24419
dc.description.abstractSelenium is essential to human health, and its deficiency is associated with different diseases including liver necrosis. Selenium is protective against viral hepatitis and hepatocellular carcinoma (HCC). The underlying molecular mechanisms of selenium effects are not well known. In this study, in vitro response of HCC-derived cell lines to selenium deficiency is examined alone or in conjunction with Vitamin E and copper/zinc. Here, we show that itt vitro selenium deficiency in a subset of HCC-derived cell lines causes oxidative stress and cytochrome c release with subsequent cell death by apoptosis. The oxidative stress and consequent cell death induced by selenium deficiency on these cells are reverted by the antioxidant effect of Vitamin E. However, most HCC cell lines (10 of 13) tolerate selenium deficiency. Consequently, they escape apoptosis. Moreover, nine of these tolerant cell lines have integrated hepatitis B Virus (HBV) DNA in their genomes, and some display p53-249 mutation, indicating past exposure to HBV or aflatoxins, established factors for oxidative stress and cancer risk in liver. An HBV-transfected clone (2.2.15) of the sensitive HepG2 cell line has gained tolerance to selenium deficiency. Our findings indicate that selenium deficiency induces apoptosis in some "hepatocyte-like" cells. However, most HCC cells, particularly HBV-related ones, tolerate selenium deficiency and escape its deadly consequences. Thus, as demonstrated by the gain of survival capacity of apoptosis-sensitive cell lines with Vitamin E, such malignant cells have acquired a selective survival advantage that is prominent under selenium-deficient and oxidative-stress conditions.en_US
dc.language.isoEnglishen_US
dc.source.titleCancer Researchen_US
dc.subjectAflatoxinen_US
dc.subjectAlpha tocopherolen_US
dc.subjectCytochrome cen_US
dc.subjectSeleniumen_US
dc.subjectApoptosisen_US
dc.subjectCancer risken_US
dc.subjectCell deathen_US
dc.subjectCell protectionen_US
dc.subjectCell survivalen_US
dc.subjectHepatitis B virusen_US
dc.subjectHumanen_US
dc.subjectHuman cellen_US
dc.subjectimmunological toleranceen_US
dc.subjectLiver cell carcinomaen_US
dc.subjectLiver necrosisen_US
dc.subjectMitochondrial respirationen_US
dc.subjectOxidative stressen_US
dc.titleAcquired tolerance of hepatocellular carcinoma cells to selenium deficiency: a selective survival mechanism?en_US
dc.typeArticleen_US
dc.departmentDepartment of Molecular Biology and Geneticsen_US
dc.citation.spage6707en_US
dc.citation.epage6715en_US
dc.citation.volumeNumber63en_US
dc.citation.issueNumber20en_US
dc.publisherAmerican Association for Cancer Researchen_US


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