AIM: To study the cell cycle alterations of human hepatoma cell line HepG(2) in vitro after (60)Co gamma-irradiation and further to examine the mechanisms underlying the enhancement of radiosensitivity to gamma-irradiation in HepG(2) transiently transfected with wild type p27(kip1). METHODS: The proliferation of HepG(2) cells was evaluated with MTT assay, and the cell cycle profile and apoptosis were assessed by cell morphology, DNA fragmentation analysis and flow cytometry. HepG(2) cells were transfected with p27(kip1) wild type by using Lipofectamine (LF2000), and the expression and subcellular localization of p27(kip1) in HepG(2) were detected by immunocytochemistry. RESULTS: (60)Co gamma-irradiation inhibited the growth of HepG(2) cells in a dose-dependent manner. Apoptosis of HepG(2) cells was induced 48 h after gamma ray exposure. Furthermore research was carried out to induce exogenous expression of p27(kip1) in HepG(2). The expression of p27(kip1) induced G(0)/G(1) phase arrest in HepG(2) cells. The overexpression of p27(kip1) enhanced (60)Co gamma-irradiation-induced radiosensitivity in HepG(2) 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.
AIM: To study the cell cycle alterations of humanhepatoma cell line HepG(2) in vitro after (60)Co gamma-irradiation and further to examine the mechanisms underlying the enhancement of radiosensitivity to gamma-irradiation in HepG(2) transiently transfected with wild type p27(kip1). METHODS: The proliferation of HepG(2) cells was evaluated with MTT assay, and the cell cycle profile and apoptosis were assessed by cell morphology, DNA fragmentation analysis and flow cytometry. HepG(2) cells were transfected with p27(kip1) wild type by using Lipofectamine (LF2000), and the expression and subcellular localization of p27(kip1) in HepG(2) were detected by immunocytochemistry. RESULTS: (60)Co gamma-irradiation inhibited the growth of HepG(2) cells in a dose-dependent manner. Apoptosis of HepG(2) cells was induced 48 h after gamma ray exposure. Furthermore research was carried out to induce exogenous expression of p27(kip1) in HepG(2). The expression of p27(kip1) induced G(0)/G(1) phase arrest in HepG(2) cells. The overexpression of p27(kip1) enhanced (60)Co gamma-irradiation-induced radiosensitivity in HepG(2) cells. CONCLUSION: Overexpression of p27(kip1) is a rational approach to improve conventional radiotherapy outcomes, which may be a possible strategy for humanhepatoma therapy.
Authors: T Takayama; T Sekine; M Makuuchi; S Yamasaki; T Kosuge; J Yamamoto; K Shimada; M Sakamoto; S Hirohashi; Y Ohashi; T Kakizoe Journal: Lancet Date: 2000-09-02 Impact factor: 79.321
Authors: Y H Huang; J C Wu; W Y Lui; G Y Chau; S H Tsay; J H Chiang; K L King; T I Huo; F Y Chang; S D Lee Journal: World J Surg Date: 2000-05 Impact factor: 3.352
Authors: K Hanazaki; S Kajikawa; N Shimozawa; M Mihara; K Shimada; M Hiraguri; N Koide; W Adachi; J Amano Journal: J Am Coll Surg Date: 2000-10 Impact factor: 6.113
Authors: M V Ponce-Castañeda; M H Lee; E Latres; K Polyak; L Lacombe; K Montgomery; S Mathew; K Krauter; J Sheinfeld; J Massague Journal: Cancer Res Date: 1995-03-15 Impact factor: 12.701