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Effects of antisense oligonucleotides of PKC-α on proliferation and apoptosis of HepG2 in vitro |
Bao-Hua Zhu, Zhen-Xiang Yao, Shao-Jun Luo, Li-Ming Jiang, Jiang-Wei Xiao, Sheng-Chun Liu, Jin-Biao Liu, Jian-Ming Sun and Zhi-Yuan Pei |
Chongqing, China
Author Affiliations: Department of Hepatobiliary Surgery, First Affiliated Hospital, Chongqing University of Medical Sciences, Chongqing 400016, China( Zhu BH, Yao ZX, Luo SJ, Jiang LM, Xiao JW, Liu SC, Liu JB, Sun JM and Pei ZY)
Corresponding Author: Bao-Hua Zhu, MD, Department of Hepatobiliary Surgery, First Affiliated Hospital, Chongqing University of Medical Sciences, Chongqing 400016, China (Tel: 86-759-2388416; Fax: 86-759-2284104; Email: baohuazhu@sohu.com) |
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Abstract BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most common malignancies in China. The long-term survival rate of patients with HCC after prevention and management remains unsatisfactory. In order to provide a novel strategy to cure HCC, we investigated the effects of antisense oligonucleotides of PKC-α on proliferation and apoptosis of human hepatoma cell line HepG2 in vitro.
METHODS: The human hepatocellular carcinoma cell line HepG2 was cultured and subcultured in RPMI1640 medium in vitro. PKC-α antisense oligonucleotides(asODN) of different concentrations with a random sequence as a control were transfected into HepG2 cells by lipofectin(LP). The cell growth index (GI) and the clone formation rate of HepG2 were detected by MTT colorimetric assay and soft agar assay, respectively. The apoptosis rate of HepG2 treated with PKC-α asODN was assayed by flow cytometry(FCM). The results were analyzed by SPSS 10.0 software.
RESULTS: The GI of HepG2 transfected by PKC-α asODN with concentrations ranging from 0.10 μmol to 1.00 μmol were lower significantly than those of control groups (P<0.05). The clone formation rates of HepG2 transfected by PKC-α asODN from 0.05 μmol to 1.00 μmol were lower significantly than those of the control groups (P<0.01), and there was a dose-dependent relationship among them. The apoptosis rates of HepG2 treated with PKC-α asODN from 0.50 μmol to 1.00 μmol were significantly higher than those of the control groups.
CONCLUSION: PKC-α asODN could inhibit the growth and proliferation of HepG2 and induce its apoptosis by blocking the cell signal transduction related to PKC-α in vitro, and may be potentially used in the prevention and management of recurrent and metastatic HCC.
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