Inhibitory effect of wild-type RASSF1A gene expression on proliferation of hepatocellular carcinoma QGY-7703 cells

BACKGROUND & OBJECTIVE: The potential molecular mechanisms of the antitumor role of Ras association domain family 1 A (RASSF1A) has not been well understood. This study was to explore the molecular mechanisms of proliferation-suppressing ability of wild type RASSF1A in hepatocellular carcinoma (HCC) QGY-7703 cells. METHODS: Vectors containing wild type or mutant RASSF1A were transfected into QGY-7703 cells. Cell cycle was determined by flow cytometry (FCM). Western blot was used to examine the protein levels of Cyclin D1, Cyclin E and P21. Luciferase activity assay was performed to study the effect of wild type RASSFIA expression on cyclin D1 promoter activity in QGY-7703 cells. Reverse transcription-polymerase chain reaction (RT-PCR) was performed to detect the mRNA level of cyclin D1. RESULTS: Wild type RASSF1A expression resulted in G1/S arrest in QGY-7703 cells, decreased the protein level of Cyclin D1, but had no effect on the protein levels of Cyclin E and P21, the promoter activity and mRNA level of cyclin D1. The exogenous expression of cyclin D1 rescued the G1 phase arrest induced by wild type RASSF1A. CONCLUSION: Wild type RASSF1A expression could induce G1 phase arrest in QGY-7703 cells, which is accompanied by a down-regulation of Cyclin D1 protein expression through a post-transcriptional mechanism.