ACC1 is overexpressed in liver cancers and contributes to the proliferation of human hepatoma Hep G2 cells and the rat liver cell line BRL 3A.

Abstract

Acetyl-coenzyme A carboxylase 1 (ACC1) serves a major role in fatty acid synthesis. Previous reports have indicated that ACC1 is a promising drug target for treating human diseases, particularly cancers and metabolic diseases; however, the role of ACC1 in liver cancer and normal liver function remains unknown. In the present study, bioinformatics analysis indicated that ACC1 is overexpressed in liver cancer. Kaplan-Meier survival analysis revealed that the expression levels of ACC1 are highly associated with the prognosis of patients with liver cancer. To determine the role of ACC1 in cancer and normal liver cells, ACC1 expression was downregulated in human hepatoma Hep G2 cells and the rat liver cell line BRL 3A using RNA interference technology, which demonstrated that silencing of ACC1 significantly suppressed the cell viability in the two cell lines. Additionally, ACC1 knockdown decreased the mRNA and protein expression levels of the cell proliferation-associated genes MYCN, JUN, cyclin D1 (CCND1) and cyclin A2 (CCNA2) in BRL 3A. Furthermore, the number of cells in division phase (G2/M) was significantly reduced in the interference group, as detected by flow cytometry. Thus, ACC1 may bind and activate CCNA2, CCND1, MYCN and JUN to promote BRL 3A proliferation. In summary, the results of present study indicated that overexpression of ACC1 is significantly associated with the survival time of patients with liver cancer, and may provide insight into the association between ACC1 and cell proliferation in BRL 3A cells.