Knockdown of GCF2/LRRFIP1 by RNAi Causes Cell Growth Inhibition and Increased Apoptosis in Human Hepatoma HepG2 Cells


Background: GC-binding factor 2 (GCF2) is a transcriptional regulator that represses transcriptional activityof the epidermal growth factor receptor (EGFR) by binding to a specific GC-rich sequence in the EGFR genepromoter. In addition to this function, GCF2 has also been identified as a tumor-associated antigen and regardedas a potentially valuable serum biomarker for early human hepatocellular carcinoma (HCC) diagnosis. GCF2is high expressed in most HCC tissues and cell lines including HepG2. This study focused on the influence ofGCF2 on cell proliferation and apoptosis in HepG2 cells. Materials and
Methods: GCF2 expression at bothmRNA and protein levels in HepG2 cells was detected with reverse transcription (RT) PCR and Western blotting,respectively. RNA interference (RNAi) technology was used to knock down GCF2 mRNA and protein expression.Afterwards, cell viability was analyzed with a Cell Counting Kit-8 (CCK-8), and cell apoptosis and caspase 3activity by flow cytometry and with a Caspase 3 Activity Kit, respectively.
Results: Specific down-regulation ofGCF2 expression caused cell growth inhibition, and increased apoptosis and caspase 3 activity in HepG2 cells.
Conclusions: These primary results suggest that GCF2 may influence cell proliferation and apoptosis in HepG2cells, and also provides a molecular basis for further investigation into the possible mechanism at proliferationand apoptosis in HCC.