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      • Department of Molecular Biology and Genetics
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      Acquired tolerance of hepatocellular carcinoma cells to selenium deficiency: a selective survival mechanism?

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      Author(s)
      Irmak, M. B.
      Ince, G.
      Ozturk, M.
      Cetin Atalay, R.
      Date
      2003
      Source Title
      Cancer Research
      Print ISSN
      0008-5472
      Publisher
      American Association for Cancer Research
      Volume
      63
      Issue
      20
      Pages
      6707 - 6715
      Language
      English
      Type
      Article
      Item Usage Stats
      157
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      28
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      Abstract
      Selenium 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.
      Keywords
      Aflatoxin
      Alpha tocopherol
      Cytochrome c
      Selenium
      Apoptosis
      Cancer risk
      Cell death
      Cell protection
      Cell survival
      Hepatitis B virus
      Human
      Human cell
      immunological tolerance
      Liver cell carcinoma
      Liver necrosis
      Mitochondrial respiration
      Oxidative stress
      Permalink
      http://hdl.handle.net/11693/24419
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