AIM: To study the cell cycle alterations of human hepatoma cell line HepG2 in vitro after ^60Co γ-irradiation and further to examine the mechanisms underlying the enhancement of radiosensitivity to γ-irradiation in ...AIM: To study the cell cycle alterations of human hepatoma cell line HepG2 in vitro after ^60Co γ-irradiation and further to examine the mechanisms underlying the enhancement of radiosensitivity to γ-irradiation in HepG2 transiently transfected with wild type p27^kip1. METHODS: The proliferation of HepG2 cells was evaluated with MTT assay, and the cell cycle profile and apoptosis were assessed by cell morphology, DNA fragmentation analysis and flow cytometry. HepG2 cells were transfectedwith p27^kip1 wild type by using Lipofectamine (LF2000), and the expression and subcellular localization of p27^kip1 in HepG2 were detected by immunocytochemistry.RESULTS: ^60Co γ-irradiation inhibited the growth of HepG2 cells in a dose-dependent manner. Apoptosis of HepG2 cells was induced 48 h after ~, ray exposure. Furthermore research was carried out to induce exogenous expression of p27^kip1 in HepG2. The expression of p27^kip1 induced G0/G1 phase arrest in HepG2 cells. The overexpression of p27^kip1 enhanced ^60Co γ-irradiation-induced radiosensitivity in HepG2 cells. CONCLUSION: Overexpression of p27^kip1 is a rational approach to improve conventional radiotherapy outcomes, which may be a possible strategy for human hepatoma therapy.展开更多
基金Supported by the National Postdoctor Research Foundation of China,No.2003034383
文摘AIM: To study the cell cycle alterations of human hepatoma cell line HepG2 in vitro after ^60Co γ-irradiation and further to examine the mechanisms underlying the enhancement of radiosensitivity to γ-irradiation in HepG2 transiently transfected with wild type p27^kip1. METHODS: The proliferation of HepG2 cells was evaluated with MTT assay, and the cell cycle profile and apoptosis were assessed by cell morphology, DNA fragmentation analysis and flow cytometry. HepG2 cells were transfectedwith p27^kip1 wild type by using Lipofectamine (LF2000), and the expression and subcellular localization of p27^kip1 in HepG2 were detected by immunocytochemistry.RESULTS: ^60Co γ-irradiation inhibited the growth of HepG2 cells in a dose-dependent manner. Apoptosis of HepG2 cells was induced 48 h after ~, ray exposure. Furthermore research was carried out to induce exogenous expression of p27^kip1 in HepG2. The expression of p27^kip1 induced G0/G1 phase arrest in HepG2 cells. The overexpression of p27^kip1 enhanced ^60Co γ-irradiation-induced radiosensitivity in HepG2 cells. CONCLUSION: Overexpression of p27^kip1 is a rational approach to improve conventional radiotherapy outcomes, which may be a possible strategy for human hepatoma therapy.
