Open AccessInhibition of Liver Carcinoma Cell Invasion and Metastasis by Knockdown of Cullin7 In Vitro and In Vivo
Author(s) -
Donghui Zhang,
Guoyu Yang,
Xidong Li,
Cheng Xu,
Honglei Ge
Publication year - 2016
Publication title -
oncology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 57
eISSN - 1555-3906
pISSN - 0965-0407
DOI - 10.3727/096504016x14519995067562
Subject(s) - ubiquitin ligase , metastasis , epithelial–mesenchymal transition , gene knockdown , cancer research , oncogene , biology , gene silencing , cullin , hepatocellular carcinoma , cancer , in vivo , mesenchymal stem cell , ubiquitin , liver cancer , pathology , cell culture , cell cycle , microbiology and biotechnology , medicine , gene , genetics
Cullin7 is an E3 ubiquitin ligase. The Cullin7 protein family functions as a molecular scaffold to coordinate substrate ubiquitination in Skp, Cullin, and F-box-containing complex (SCF complex). Cullin7s control normal development and primary cellular processes and are characterized by a unique genomic network organization. Less is known about the involvement of Cullin7 with hepatocellular carcinoma (HCC). In this study, we found that Cullin7 showed a high expression in HCC tumor tissues, especially in metastatic HCC tumor tissues. Also, there was a negative correlation between Cullin7 expression and long survival. Silencing of Cullin7 in liver cancer cells can significantly reduce the migration, invasion, and metastatic abilities. Also, detection of epithelial-mesenchymal transition (EMT) marker expression showed that Cullin7 promotes epithelial-mesenchymal transformation of cancer cells. The results of this study helped to elucidate the oncogene functions of Cullin7 in liver cancers.