AIM:To study the cell cycle alterations of human hepatomacell line HepG2in vitro after60Co γ-irradiation and furtherto examine the mechanisms underlying the enhancementof radiosensitivity to γ-irradiation in HepG2transientlytransfected with wild type p27kipl.METHODS:The proliferation of HepG2cells was evaluatedwith MTT assay,and the cell cycle profile and apoptosiswere assessed by cell morphology,DNA fragmentationanalysis and flow cytometry.HepG2cells were transfectedwith p27kip1wild type by using Lipofectamine(LF2000),andthe expression and subcellular localization of p27kip1in HepG2were detected by immunocytochemistry.RESULTS:60Co γ-irradiation inhibited the growth of HepG2cells in a dose-dependent manner.Apoptosis of HepG2cellswas induced 48 h after γ ray exposure.Furthermore researchwas carried out to induce exogenous expression of p27kip1in HepG2.The expression of p27kip1induced G0/G1phasearrest in HepG2cells.The overexpression of p27kip1enhanced60Co γ-irradiation-induced radiosensitivity in HepG2cells.CONCLUSION:Overexpression of p27kip1is a rational approachto improve conventional radiotherapy outcomes,which maybe a possible strategy for human hepatoma therapy.Guan XX,Chen LB,Ding GX,De W,Zhang AH.Transfection ofp27kip1enhances radiosensitivity induced by60Co γ-irradiation inhepatocellular carcinoma HepG2cell line.World J Gastroenterol2004;10(21):3103-3106http://www.wjgnet.com/1007-9327/10/3103.asp