Decreased Tumorigenicity In Vivo When Transforming Growth Factor .BETA. Treatment Causes Cancer Cell Senescence

  • KATAKURA Yoshinori
    <i>Department of Genetic Resources Technology, Faculty of Agriculture, Kyushu University</i>
  • NAKATA Eriko
    <i>Department of Genetic Resources Technology, Faculty of Agriculture, Kyushu University</i>
  • TABIRA Yukiko
    <i>Department of Genetic Resources Technology, Faculty of Agriculture, Kyushu University</i>
  • MIURA Takumi
    <i>Department of Genetic Resources Technology, Faculty of Agriculture, Kyushu University</i>
  • TERUYA Kiichiro
    <i>Department of Genetic Resources Technology, Faculty of Agriculture, Kyushu University</i>
  • TSUCHIYA Toshie
    <i>Division of Medical Devices, National Institute of Health Sciences</i>
  • SHIRAHATA Sanetaka
    <i>Department of Genetic Resources Technology, Faculty of Agriculture, Kyushu University</i>

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Other Title
  • Decreased Tumorigenicity In Vivo When Transforming Growth Factor β Treatment Causes Cancer Cell Senescence
  • Decreased Tumorigenicity In Vivo When Transforming Growth Factor ベータ Treatment Causes Cancer Cell Senescence
  • Decreased Tumorigenicity<i>In Vivo</i>When Transforming Growth Factor β Treatment Causes Cancer Cell Senescence

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Abstract

  We have previously reported that transforming growth factor β (TGF-β) triggers two independent senescence programs, 1) replicative senescence dependent upon telomere shortening and 2) premature senescence independent of telomere shortening, in the cell line of A549 human lung adenocarcinoma. In this study, we examined the possibility that cancer cell tumor phenotypes could be suppressed by forced senescence. We used A549 cells treated with TGF-β for a long time (over 50 days), where senescence was induced in a telomere-shortening-dependent or an independent way. Fully senescent A549 cells were elongated, acquired contact inhibition capabilities when reaching confluence, and secreted the senescence-associated cytokine IL-6. Furthermore, senescent A549 cells had no tumorigenicity in nude mice. These results indicate that the forced induction of senescence in cancer cells may be a novel and potentially powerful method for advancing anti-cancer therapy.<br>

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