Recombinant human decorin upregulates p57KIP² expression in HepG2 hepatoma cell lines.

Increasing the expression of cyclin-cyclin-dependent kinase inhibitors (cyclin-CDK) using small molecule inhibitors is a therapeutic strategy used to suppress cancer cell growth. Decorin (DCN), a functional component of the extracellular matrix, has been implicated in the suppression of cell proliferation by upregulating p21, a cyclin-CDK inhibitor. The purpose of this study was to examine the effect of recombinant decorin on the reactivation of p57KIP2, whose expression is silenced in hepatocellular carcinoma (HCC).

Aflatoxin B1-induced hepatocellular carcinoma in developing countries: Geographical distribution, mechanism of action and prevention.

Hepatocellular carcinoma (HCC) is the most well-known primary liver malignancy worldwide. Its incidence is rising at alarming rates and has become a public concern globally. It is more frequent in developing countries than in industrialized countries with respect to geographical variation, ethnic disparities and socioeconomic status.

Recombinant human decorin suppresses liver HepG2 carcinoma cells by p21 upregulation.

Background: Decorin is a multifunctional molecule of the extracellular matrix and impedes different kinds of tumor cell growth, but the role and molecular mechanism by which decorin inhibits HepG2 cells is not fully understood. Our objective was to construct recombinant human decorin (pcDNA3.1-DCN) and to explore the mechanism by which it inhibits HepG2 cells.