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KMID : 1140120090140040335
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Cancer Prevention Research
2009 Volume.14 No. 4 p.335 ~ p.341
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Antitumor Effects of the Selenium in Human Papillomavirus 16 (E6/E7) Immortalized TC-1 Cell Line and Animal Model
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Kim Yong-Wook
Wen Ran-Ying
Bae Su-Mi
Bae Si-Hyun
Seo Young-Rok
Ahn Woong-Shick
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Abstract
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Selenium is an essential trace element and has anticarcinogenic properties. In this study, we investigated the anticancer effects of selenium on human papillomavirus 16 (E6/E7) immortalized TC-1 cell line and animal model. For this, the effects of selenium on growth inhibition, apoptosis and cell cycle, PCR array were examined and also tumor growth inhibition study was evaluated. Cell viability assay of TC-1 cell line was measured using MTT assay and morphological change was observed with microscope. For apoptosis and cell cycle analysis, Annexin V-FITC/PI staining was performed and FACS analysis. Also, quantitative PCR array was performed to assay the signal transduction regulation. Additionally, this study was supported by the finding that selenium shows a inhibition effect of tumor growth in C57BL/6 mice with TC-1 cells xenographs in vivo. Selenium inhibited the growth of TC-1 cell line and induced apoptosis. Also selenium was arrest cell cycle at S and G2/M phase. In signal transduction pathway Superarray, genes closely relate to NF?B, NFAT (nuclear factor of activated T-cell), Jak-Stat and LDL (Low-density lipoprotein) pathway such as Cxcl1, Icam1, Il1a, Il2, Lta (TNFb), Nfkbia, Nos2 (iNOS) and Tnf (TNFa) were very significantly up or down-regulated in TC-1 cell following treatment of selenium. In TC-1 tumor-bearing mouse model, selenium was also effective in tumor suppression as well as in vitro tumor suppression results. These studies showed that selenium could sufficiently inhibited tumor cell proliferation and effectively induce tumor suppression. These effects may be due to regulation of signal trasduction pathway related genes. Therefore we suggest that selenium can be an approach to induce effective anti- cancer effects.
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KEYWORD
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Selenium, Cervical cancer, Apoptosis, Signal transduction pathway
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