Knockdown of GCF2/LRRFIP1 by RNAi Causes Cell Growth Inhibition and Increased Apoptosis in Human Hepatoma HepG2 Cells
| Autor: | Xiao-Xun Xie, Shao-Jian He, Bo Wu, Ping Ma, Ri-Ting Jiang, Su-Fang Zhou, Tianming Huang, Nai-Xia Cao, Jing-Ping Li, Guo-Rong Luo, Defeng Chen, Li Chen |
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| Rok vydání: | 2014 |
| Předmět: |
Cancer Research
Carcinoma Hepatocellular Epidemiology Blotting Western Apoptosis Biology Real-Time Polymerase Chain Reaction Flow cytometry RNA interference Tumor Cells Cultured medicine Humans RNA Messenger Viability assay RNA Small Interfering Promoter Regions Genetic Cell Proliferation Gene knockdown medicine.diagnostic_test Reverse Transcriptase Polymerase Chain Reaction Cell growth Liver Neoplasms Public Health Environmental and Occupational Health RNA-Binding Proteins Flow Cytometry Molecular biology Gene Expression Regulation Neoplastic Oncology Cell culture A431 cells |
| Zdroj: | Asian Pacific Journal of Cancer Prevention. 15:2753-2758 |
| ISSN: | 1513-7368 |
| DOI: | 10.7314/apjcp.2014.15.6.2753 |
| Popis: | Background: GC-binding factor 2 (GCF2) is a transcriptional regulator that represses transcriptional activity of the epidermal growth factor receptor (EGFR) by binding to a specific GC-rich sequence in the EGFR gene promoter. In addition to this function, GCF2 has also been identified as a tumor-associated antigen and regarded as a potentially valuable serum biomarker for early human hepatocellular carcinoma (HCC) diagnosis. GCF2 is high expressed in most HCC tissues and cell lines including HepG2. This study focused on the influence of GCF2 on cell proliferation and apoptosis in HepG2 cells. Materials and Methods: GCF2 expression at both mRNA 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 3 activity by flow cytometry and with a Caspase 3 Activity Kit, respectively. Results: Specific down-regulation of GCF2 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 HepG2 cells, and also provides a molecular basis for further investigation into the possible mechanism at proliferation and apoptosis in HCC. |
| Databáze: | OpenAIRE |
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