A research article published on January 28, 2011 in the World Journal of Gastroenterology addresses this question. In this study, the authors investigated the expression profile of E2F5 in primary HCCs and explored the biological effects of E2F5 overexpression by knockdown of the gene.
This is the first evidence that E2F5 is commonly overexpressed in primary human HCC and that E2F5 knockdown profoundly repressed the growth of HCC cells. The overexpression of E2F5 may induce uncontrollable cell cycle progression in liver cells and eventually contribute to cancer transformation by working together with other carcinogenic factors. This study will help to understand hepatocarcinogenesis mechanisms and to define therapeutic targets of early HCC.
Read the complete press release..............