Effect of HCCR-2 antisense-nucleic acids on biological behaviour of HepG2 hepatocellular carcinoma cells
Zhang Shurong
Abstract
Zhang Shurong
Abstract
ObjectiveTo study the effect of HCCR-2 antisense-nucleic acids on biological behaviour of HepG2 hepatocellular carcinoma cells by utilizing the constructed antisense recombinant eukaryotic expression vector of pIRES2-EGFP/HCCR2 (-). MethodsChanges of HepG2 transfected by pIRES2-EGFP/HCCR-2(-) were detected by MTT,FCM,plate clone formation methods and cell migration experiment respectively. ResultsThe cell proliferation ability,proliferative index,single cell clone formation capacity,and cell migration of HepG2-H cells were significant lower than those of HepG2 and HepG2-P cells.In addition,the growth of HepG2-H cells was blocked in G0/G1 stage. ConclusionThe proliferative speed,single cell clone formation capacity,and cell migration capacity in vitro of HepG2 hepatoma carcinoma cells can be effectively inhibited by HCCR-2 antisense-nucleic acids by using antisense recombinant eukaryotic expression vector.
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ObjectiveTo study the effect of HCCR-2 antisense-nucleic acids on biological behaviour of HepG2 hepatocellular carcinoma cells by utilizing the constructed antisense recombinant eukaryotic expression vector of pIRES2-EGFP/HCCR2 (-). MethodsChanges of HepG2 transfected by pIRES2-EGFP/HCCR-2(-) were detected by MTT,FCM,plate clone formation methods and cell migration experiment respectively. ResultsThe cell proliferation ability,proliferative index,single cell clone formation capacity,and cell migration of HepG2-H cells were significant lower than those of HepG2 and HepG2-P cells.In addition,the growth of HepG2-H cells was blocked in G0/G1 stage. ConclusionThe proliferative speed,single cell clone formation capacity,and cell migration capacity in vitro of HepG2 hepatoma carcinoma cells can be effectively inhibited by HCCR-2 antisense-nucleic acids by using antisense recombinant eukaryotic expression vector.
Key concepts: clone (Java method), Transfection, Nucleic acid, Recombinant DNA, Molecular biology, Cell growth, Cell, Hepatocellular carcinoma