کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2112884 | 1084428 | 2013 | 9 صفحه PDF | دانلود رایگان |

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.
► We developed a dual expression plasmid that coexpressed-E6-specific siRNA and wild type p53.
► Simultaneous expression of pSi-E6-P53 caused a robust suppression of tumor growth.
► A combined strategy of co-expressed E6-siRNA and p53 more effectively suppressed cervical tumor growth.
Journal: Cancer Letters - Volume 335, Issue 1, 10 July 2013, Pages 242–250