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      Tamoxifen induces oxidative stress and apoptosis in oestrogen receptor-negative human cancer cell lines

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          Abstract

          Recent data have demonstrated that the anti-oestrogen tamoxifen (TAM) is able to facilitate apoptosis in cancer cells not expressing oestrogen receptor (ER). In an attempt to identify the biochemical pathway for this phenomenon, we investigated the role of TAM as an oxidative stress agent. In two ER-negative human cancer cell lines, namely T-leukaemic Jurkat and ovarian A2780 cancer cells, we have demonstrated that TAM is able to generate oxidative stress, thereby causing thiol depletion and activation of the transcriptional factor NF-κB. As described for other oxidative agents, TAM was able to induce either cell proliferation or apoptosis depending on the dose. When used at the lowest dose tested (0.1 μ M), a slight proliferative effect of TAM was noticed in terms of cell counts and DNA synthesis rate, whereas at higher doses (10 μ M) a consistent occurrence of apoptosis was detected. Importantly, the induction of apoptosis by TAM is not linked to down-regulation or functional inactivation by phosphorylation of the antiapoptotic bcl-2 protein. © 1999 Cancer Research Campaign

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          Author and article information

          Journal
          Br J Cancer
          British Journal of Cancer
          Nature Publishing Group
          0007-0920
          1532-1827
          January 1999
          : 79
          : 2
          : 257-263
          Affiliations
          [1 ]Laboratory of Antineoplastic Pharmacology, Zeneca, and Department of Obstetrics and Gynecology, Catholic University of Sacred Heart, Rome, Italy
          Author notes
          [* ]Author for correspondence:
          Article
          6690042
          10.1038/sj.bjc.6690042
          2362195
          9888466
          Copyright 1999, Cancer Research Campaign
          Categories
          Regular Article

          Oncology & Radiotherapy

          oxidative stress, tamoxifen, apoptosis, nf-κb

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