Plasmid-based E6-specific siRNA and co-expression of wild-type p53 suppresses the growth of cervical cancer in vitro and in vivo.

Plasmid-based E6-specific siRNA and co-expression of wild-type p53 suppresses the growth of cervical cancer in vitro and in vivo.
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DOI:
10.1016/j.canlet.2013.02.034
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发表时间:
2013-07-10
期刊:
影响因子:
9.7
通讯作者:
Zhang, Ling
Zhang, Ling
中科院分区:
医学1区
文献类型:
--
作者:
Li, Xin;Li, Yang;Hu, Jiadi;Wang, Bo;Zhao, Lijing;Ji, Kun;Guo, Baofeng;Yin, Di;Du, Yanwei;Kopecko, Dennis J.;Kalvakolanu, Dhananjaya V.;Zhao, Xuejian;Xu, Deqi;Zhang, Ling

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致癌HPV-16的E6蛋白通过干扰正常的细胞周期控制机制,特别是那些由p53控制的机制来发挥作用。在这项研究中,我们开发了一个双表达质粒,共表达E6特异性siRNA和野生型p53,并评估其对宫颈癌生长的影响。我们发现,与对照组E6特异性siRNA或单独的p53相比,pSi-E6-P53的同时表达引起了对肿瘤生长的强烈抑制。总之,我们的研究结果表明,与单一治疗相比,E6特异性siRNA和p53共表达的联合策略协同作用,更有效地抑制宫颈肿瘤生长。
The E6 protein of the oncogenic HPV-16 functions by interfering with the normal cell cycle control mechanisms, particularly those controlled by p53. In this study, we developed a dual expression plasmid that coexpressed-E6-specific siRNA and wild type p53, and to evaluate its effects on cervical cancer growth. We found that simultaneous expression of pSi-E6-P53 caused a robust suppression of tumor growth when compared to the controls either E6-specific siRNA or p53 alone. In conclusion, our findings demonstrate that a combined strategy of co-expressed E6-specific siRNA and p53 synergistically and more effectively suppressed cervical tumor growth when compared with single treatment.
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