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논문 기본 정보

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학술저널
저자정보
Li, Jing-Ping (Department of Histology and Embryology, School of Preclinical Medicine, Guangxi Medical University) Cao, Nai-Xia (Department of Histology and Embryology, School of Preclinical Medicine, Guangxi Medical University) Jiang, Ri-Ting (Department of Histology and Embryology, School of Preclinical Medicine, Guangxi Medical University) He, Shao-Jian (Department of Histology and Embryology, School of Preclinical Medicine, Guangxi Medical University) Huang, Tian-Ming (Department of Histology and Embryology, School of Preclinical Medicine, Guangxi Medical University) Wu, Bo (Department of Histology and Embryology, School of Preclinical Medicine, Guangxi Medical University) Chen, De-Feng (Department of Histology and Embryology, School of Preclinical Medicine, Guangxi Medical University) Ma, Ping (Department of Histology and Embryology, School of Preclinical Medicine, Guangxi Medical University) Chen, Li (Department of Histology and Embryology, School of Preclinical Medicine, Guangxi Medical University) Zhou, Su-Fang (Department of Histology and Embryology, School of Preclinical Medicine, Guangxi Medical Uni) Xie, Xiao-Xun Luo, Guo-Rong
저널정보
아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제15권 제6호
발행연도
2014.1
수록면
2,753 - 2,758 (6page)

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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.

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