Sensitivity of anticancer drugs in NIH3T3' cells transfected with oncogenes accompanied by pSV2neo vector.

转染 分子生物学 生物 细胞培养 顺铂 遗传学 化疗
作者
Xianshu Gao,Junichi Asaumi,Shoji Kawasaki,Koji Nishikawa,Masahiro Kuroda,Yoshito Takeda,Yoshio Hiraki,Masataka Ihara,Teppei Ohnishi
出处
期刊:PubMed [National Institutes of Health]
卷期号:15 (5B): 1911-4 被引量:15
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摘要

NIH3T3 cells and NIH3T3 cell lines, which were transfected with several oncogenes accompanied by pSV2neo vector, were observed for their survival rate when treated with commonly used anticancer drugs. The survival rates in the cell line transfected with the pSV2neo vector only did not differ significantly from that of parental NIH3T3 cells against bleomycin, nimustine and adriamycin, but it was significantly more resistant to cisplatin and more sensitive to mitomycin C. Therefore, the survival rate in each transfectant was compared with that in the pSV2neo transfectant. The Val-12, v-Ha-ras, v-int-2, v-erbB or v-abl transfectants accompanied by pSV2neo vector were significantly more sensitive to cisplatin than transfection with pSV2neo vector only. The Val-12, v-Ha-ras, v-int-2 and v-abl transfectants were significantly more sensitive, and the v-erbB transfectant more resistant to bleomycin than the pSV2neo transfectant. The v-int-2, v-erbB, frg, v-raf and v-myc transfectants were more sensitive, and the v-Ha-ras transfectant more resistant to nimustine than the pSV2neo transfectant. The N-ras, v-Ha-ras, v-sis, v-int, v-abl and v-myc transfectants were significantly more sensitive to adriamycin than the pSV2neo transfectant. The v-sis and v-int-2 transfectants were more sensitive, and the c-Ki-ras, Val-12, v-erbB and the v-src transfectants more resistant to mitomycin C than the pSV2neo transfectant. Thus there was no relationship between the drug sensitivity and the location of oncogenes, but the transfection was associated with either increased or decreased sensitivity to a number of commonly used anticancer drugs. Therefore, it may be important to take into consideration or overexpression of oncogenes in cancer chemotherapy.

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