To investigate the effect of recombinant human p53 adenovirus injection combined with paclitaxel on human cervical cancer HeLa cell proliferation, apoptosis and expression of vascular endothelial growth factor (VEGF).
These data suggest that there are significant associations between the miR-502-binding site SNP in the 3'-UTR of SET8 and the TP53 codon 72 polymorphism with cervical cancer in Chinese, and there is a gene-gene interaction.
1) To analyze the expression of Ki-67, p53 and p16(INK4a) in cervical cancer, 2) to correlate the relative expression of these proteins as well as clinical parameters with the stage of disease, and 3) to determine the HPV DNA prevalence and subtype distribution.
In conclusion, Arginine at codon72 of p53 and GG genotype at 309 in P2 of MDM2 together reveal a direct proportionality with the tumor grade of cervical cancer along with HPV infection in postmenopausal women.
Among the six hot-spot codons of TP53 gene, three codons (175, 248 and 273) were the most commonly mutated in both types of cervical cancer, one codon (249) mainly in squamous cell carcinoma and one codon (282) only in adenocarcinoma.
Results from the current meta-analysis suggests that p53 codon 72 polymorphism might be associated with increased risk of cervical cancer, especially among Indians.
Here we report that differential regulation of pro- and anti-p53 setups not only upregulates p53 transcription but also stabilizes and activates p53 protein to ensure p53-induced apoptosis in HPV-18-infected cervical cancer.
Although the p53 arginine allele is itself an important risk factor for cervical cancer, the combined risk with LOH of Rb, which appears to be greater, might indicate a possible epistatic effect of the two genes/polymorphisms.
This association was not seen in HPV-negative individuals. p53Arg72Pro was not associated with the risk of cervical cancer or initiation of SIL in either HPV-positive or HPV-negative patient subsets.
Cervical cancer is caused by human papilloma virus (HPV) expressing E6 and E7 oncoproteins, which are known to inactivate tumor suppressor proteins p53 and pRb, respectively.
In conclusion, this study provides evidence for elevated LAP2α expression in cervical cancer and suggests that E2F and p53 activities associate with the positive and negative regulation of LAP2α expression, respectively.
In additional, interaction between these p53 and p21 polymorphisms increased the risk of cervical cancer in a multiplicative manner, with the OR being 3.96 (95% CI, 1.51-10.41) for subjects carrying both p53 Arg/Arg and p21 Ser/Ser genotypes.
The intratumoral delivery of exogenous E1A carried by SDION increases p53 expression but inhibits HER-2/neu expression, and enhances the radiosensitivity of human cervical cancer in xenograft mice.
Thus, polymorphism of the p53 itself as well as in combination with HPV infection may not be a genetic risk for cervical cancer and therefore much attention should be paid to other risk factors such as sexual behavior and smoking.