转导(生物物理学)
生物
卵巢癌
细胞培养
癌症研究
克隆形成试验
癌细胞
分子生物学
细胞生长
生长抑制
癌症
遗传学
生物化学
作者
Y. Kawakami,Seiji Hama,Masamichi Hiura,Takayoshi Nogawa,Take Chiba,Takashi Yokoyama,Shigemitsu Takashima,Hisao Tajiri,Kenji Eguchi,Nobutaka Nagai,Kazushi Shigemasa,Koso Ohama,Kaoru Kurisu,Yuji Heike
出处
期刊:Anticancer Research
[Anticancer Research USA Inc.]
日期:2001-07-01
卷期号:21 (4A): 2537-45
被引量:4
摘要
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.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).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.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.
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