作者: Mitsuo Yoshinouchi , Taketo Yamada , Masahiro Kizaki , Jin Fen , Takeyoshi Koseki
DOI: 10.1016/J.YMTHE.2003.08.004
关键词:
摘要: Human papillomavirus type 16 (HPV16), a causative agent of cervical cancers, encodes the E6 and E7 oncogenes, whose simultaneous expression is pivotal for malignant transformation maintenance phenotypes. In hope developing gene-specific therapy HPV-related cancer, we examined effects short-interfering RNA (siRNA) on these oncogenes cell growth HPV16-related cancer cells. Using SiHa cells, demonstrated that siRNA decreased levels mRNA encoding as well protein also induced nuclear accumulation p53, most important target E6. suppressed monolayer anchorage-independent which was associated with p21CIP1/WAF1 induction hypophosphorylation retinoblastoma protein. Further, cells treated formed tumors in NOD/SCID mice were significantly smaller than those control siRNA. Our results show HPV candidate cancer.