HPV16E7-Specific siRNA Inhibits Cell Proliferation in CaSki Cells

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• 作者：Jun-guo Li (1)
  Li Li (2)
  Shui-wen Zhang (1)
  Xiaoguang Wei (3)
  
  1. Reproductive Medicine Center ; General Hospital of Beijing Military Region ; Beijing ; 100700 ; China
  2. Institute of Field Surgery of Daping Hospital ; Third Military Medical University ; Chongqing ; 400042 ; China
  3. Department of Obstetrics and Gynecology ; General Hospital of Beijing Military Region ; Beijing ; 100700 ; China
  
• 关键词：HPV ; siRNA ; Cervical carcinomas ; E7 gene
• 刊名：Cell Biochemistry and Biophysics
• 出版年：2015
• 出版时间：March 2015
• 年：2015
• 卷：71
• 期：2
• 页码：529-534
• 全文大小：1,517 KB
• 参考文献：1. Scheffner, M., & Whitaker, N. J. (2003). Human papillomavirus-induced carcinogenesis and the ubiquitin鈥損roteasome system. / Cancer Biology, / 13, 59鈥?7. CrossRef
  2. Scheurer, M. E., Tortolero-Luna, G., Adler-Storthz, K., et al. (2005). Human papillomavirus infection: Biology, epidemiology, and prevention. / International Journal of Gynecological Cancer, / 15, 727鈥?46. CrossRef
  3. Smotkin, D., & Wettstein, F. O. (1986). Transcription of human papillomavirus type 16 early genes in a cervical cancer and a cancer-derived cell line and identification of the E7 protein. / Proceedings of the National Academy of Sciences of the United States of America, / 83, 4680鈥?684. CrossRef
  4. Elbashir, S. M., Harborth, J., Lendeckel, W., Yalcin, A., Weber, K., & Tuschl, T. (2001). Duplexes of 21-nucleotide RNAs mediate RNA interference in cultured mammalian cells. / Nature, / 411, 494鈥?98. CrossRef
  5. Hong, D., Lu, W., Ye, F., Hu, Y., & Xie, X. (2009). Gene silencing of HPV16 E6/E7 induced by promoter-targeting siRNA in SiHa cells. / British Journal of Cancer, / 101, 1798鈥?804. CrossRef
  6. Sima, N., Wang, W., Kong, D., Deng, D., Xu, Q., Zhou, J., et al. (2008). RNA interference against HPV16 E7 oncogene leads to viral E6 and E7 suppression in cervical cancer cells and apoptosis via upregulation of Rb and p53. / Apoptosis, / 13, 273鈥?81. CrossRef
  7. Denny, L. (2005). The prevention of cervical cancer in developing countries. / BJOG, / 112, 1204鈥?212. CrossRef
  8. Santin, A. D. (2005). Gene expression profiles of primary HPV16- and HPV18-infected early stage cervical cancers and normal cervical epithelium: Identification of novel candidate molecular markers for cervical cancer diagnosis and therapy. / Virology, / 331, 269鈥?91. CrossRef
  9. Unger, E. R. (2004). Human papillomavirus and cervical cancer. / Emerging Infectious Diseases, / 10, 2031鈥?032. CrossRef
  10. Dallenbach-Hellweg, G. (2004). Traditional and new molecular methods for early detection of cervical cancer. / Arkh-Patol, / 66, 35鈥?9.
  11. Gao, Q., Singh, L., Kumar, A., et al. (2001). Human papillomavirus type 16 E6 induced degradation of E6 TP1 correlates with it鈥檚 ability to immortalize human mammary epit helial cells. / Journal of Virology, / 75, 4459鈥?466. CrossRef
  12. Yoshinouchi, M., Yamada, T., Kizaki, M., et al. (2003). In vitro and in vivo growth suppression of human papillomavirus 16-positive cervical cancer cells by E6 siRNA. / Molecular Therapy, / 8, 762鈥?68. CrossRef
  
• 刊物主题：Biochemistry, general; Pharmacology/Toxicology; Biotechnology; Cell Biology; Biophysics and Biological Physics;
• 出版者：Springer US
• ISSN：1559-0283

文摘

High-risk human papilloma virus (HPV) infection is the main cause for the genesis of cervical carcinomas. After infection, E6 and E7 genes of HPV were integrated to the genome of the cervical epithelium. Continued expression of the transforming oncoproteins E6 and E7 not only drives the neoplastic progression in cervical epithelium, but also plays an important role in maintaining the malignant phenotype of cervical cancer cells. The aim of this study is to explore the effects of liposomal transfection of HPV16E7 siRNA on the proliferation of cervical carcinoma cell line CaSki. The siRNA interfering HPV16E7 gene was synthesized and transfected into CaSki cells by liposome to observe the cell morphology changes under microscope. The cell proliferation index was detected by flow cytometry; HPV16E7 mRNA expression was determined by RT-PCR and its protein level was determined by Western blot. After transfection of the CaSki cell by siRNA, cell proliferation was inhibited significantly, and the expression of HPV16E7 mRNA and protein level of HPV16E7 decreased. HPV16E7 siRNA is able to inhibit growth of CaSki cells. HPV16E7 might become a new target for genetic therapy of cervical carcinoma.