Adenovirus-mediated p16 gene transfer changes the sensitivity to taxanes and vinca alkaloids of human ovarian cancer cells

Y. Kawakami, S. Hama, M. Hiura, T. Nogawa, T. Chiba, T. Yokoyama, S. Takashima, H. Tajiri, K. Eguchi, N. Nagai, K. Shigemasa, K. Ohama, K. Kurisu, Y. Heike

研究成果: Article査読

15 被引用数 (Scopus)

抄録

Background: Deletions and point mutations of the p16 gene are detectable in more than 50% of ovarian cancer cells. In this study, we examined the effect of p16 gene transduction on the growth of ovarian cancer cells and on the effect of anti-cancer agents. Materials and Methods: p16-null human ovarian cancer cell lines, SKOV-3 and OVCAR-5, were used in this study. We transduced the full-length human p16 gene using recombinant adenovirus (AxCA-hp16). Results: The spontaneous growth of these cells was significantly inhibited by hp16 transduction. MTT assay revealed that AxCA-hp16 infection induced chemoresistance in both cell lines. Flow cytometric analysis revealed that only hp16-transduced SKOV-3, were arrested at the G1-phase for 3 days whereas those infected with AxCA-mock and OVCAR-5 infected with both recombinant viruses did not. Western blot analysis showed increased microtubule-associated proteins 4 (MAP4) in both cell lines. Conclusion: These results suggest that in SKOV-3 cells, G1-arrest induced by p16-transduction prevents paclitaxel- and vindesine- induced cell death, and in OVCAR-5 cells, the other unknown mechanisms play a role of chemoresistance.

本文言語English
ページ(範囲)2537-2546
ページ数10
ジャーナルAnticancer research
21
4 A
出版ステータスPublished - 2001
外部発表はい

ASJC Scopus subject areas

  • 腫瘍学
  • 癌研究

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