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.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.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.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.