Abstract
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.
Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.
Publication types
-
Research Support, N.I.H., Extramural
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Apoptosis
-
Apoptosis Regulatory Proteins / metabolism
-
Cell Line, Tumor
-
Cell Movement
-
Cell Proliferation*
-
Cell Survival
-
Female
-
Gene Expression
-
Gene Knockdown Techniques
-
Genetic Therapy / methods
-
Humans
-
Mice
-
Mice, Inbred BALB C
-
Mice, Nude
-
Neoplasm Transplantation
-
Oncogene Proteins, Viral / genetics*
-
Oncogene Proteins, Viral / metabolism
-
Papillomavirus Infections / metabolism
-
Papillomavirus Infections / pathology
-
Papillomavirus Infections / therapy*
-
Plasmids / genetics
-
RNA, Small Interfering / genetics*
-
Repressor Proteins / genetics*
-
Repressor Proteins / metabolism
-
Salmonella typhimurium / genetics
-
Transformation, Bacterial
-
Tumor Burden
-
Tumor Suppressor Protein p53 / genetics
-
Tumor Suppressor Protein p53 / metabolism*
-
Uterine Cervical Neoplasms / metabolism
-
Uterine Cervical Neoplasms / pathology
-
Uterine Cervical Neoplasms / therapy*
Substances
-
Apoptosis Regulatory Proteins
-
E6 protein, Human papillomavirus type 16
-
Oncogene Proteins, Viral
-
RNA, Small Interfering
-
Repressor Proteins
-
TP53 protein, human
-
Tumor Suppressor Protein p53