Author/Authors :
Yokomizo، نويسنده , , Chihiro and Yamaguchi، نويسنده , , Kanji and Itoh، نويسنده , , Yoshito and Nishimura، نويسنده , , Takeshi and Umemura، نويسنده , , Atsushi and Minami، نويسنده , , Masahito and Yasui، نويسنده , , Kohichiroh and Mitsuyoshi، نويسنده , , Hironori A. Fujii، نويسنده , , Hideki and Tochiki، نويسنده , , Nozomi and Nakajima، نويسنده , , Tomoki and Okanoue، نويسنده , , Takeshi and Yoshikawa، نويسنده , , Toshikazu، نويسنده ,
Abstract :
P300 impacts the transcription of several genes involved in biological behavior of human malignancies including hepatocellular carcinomas (HCC). We found p300 is highly expressed in 47% of surgically resected HCC specimens by immunohistochemistry, which correlated with advanced TNM staging (P = 0.034), vascular invasion (P = 0.036), intrahepatic metastasis (P = 0.001) and shortened overall survival (P = 0.028). In vitro study, knocking down of p300 expression in hepatoma cells recovered E-cadherin expression, inhibited the translocation of beta (β)-catenin into the nuclei, decreased cyclin D1 activity and suppressed the migration/invasion of HCC cells. Furthermore, suppression of p300 led to down-regulation of epithelial-mesenchymal transition (EMT)-related molecules such as Snail, Twist and HIF-1 alpha. These observations suggest that p300 contributes to the EMT-related progression of HCCs.
Keywords :
Overall survival , E-Cadherin , tumor invasion , HCC , P300
