ABSTRACT
Objective To investigate the expression and significance of β-catenin and p28GANK in residual hepatocellular carcinoma (HCC)cells after transcatheter arterial chemoembolization (TACE).Methods We collected forty-five cases of surgical specimens of hepatocellular carcinoma after TACE ( TACE group ) and thirty cases of surgery without any treatment (pure surgery group).The expression of β-catenin and p28GANK were detected by using immunohistochemical SP method and compared between the two groups .Results The positive expression of β-catenin and p28GANK in TACE group were 77.78%and 75.56%respectively,which were significantly higher than those in pure surgery group (46.67%and 53.33%respectively,P<0.05).In the residual hepatocellular carcinoma cells of TACE group ,the positive expression of β-catenin showed correlation with the positive expression of p28GANK(Φ=0.318,P =0.033).The high expression of β-catenin and p28GANK were closely related to portal vein thrombosis and distant metastasis (P<0.05).Conclusion The ex-pression of β-catenin and p28GANK in the residual hepatocellular carcinoma cells were increased significantly after TACE.The high expression of β-catenin and p28GANK were closely related to portal vein thrombosis and distant metastasis.The high expression of β-catenin and p28GANK may be one of the reasons of hepatocellular carcinoma invasiveness and metastasis .
ABSTRACT
Objective: To construct the mutants of oncogene p28GANK with different ankyrin repeats deleted, so as to further study the potential role of p28GANK in hepatocellular carcinoma (HCC). Methods: QuikChang Site-Directed Mutagenesis Kit was used to construct five p28GANK mutants with different ankyrin repeats deleted and their influences on p53 were also investigated. Results: Five deletion mutants of p28GANK were as follows: 39-71aa, 72-104aa, 105-137aa, 138-170aa, and 171-203aa. Agarose gel electrophoresis and Western blotting analysis confirmed the correct construction of these mutants. Wild type p28GANK promoted degradation of p53, but the 5 mutants had no noticeable effects on expression of p53. Conclusion: We have successfully constructed five p28GANK ankyrin repeat-deleted mutants. It is confirmed that the regulation of p53 needs the complete ankyrin repeats of p28GANK, which paves a way for further research on ankyrin and the role of p28GANK in HCC.