Open AccessSensitivity of human glioma U‐373MG cells to radiation and the protein kinase C inhibitor, calphostin C
Author(s) -
AcevedoDuncan M.,
Pearlman J.,
Zachariah B.
Publication year - 2001
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1046/j.1365-2184.2001.00194.x
Subject(s) - calphostin c , radiosensitivity , cell cycle , radiation sensitivity , cell growth , microbiology and biotechnology , biology , glioma , cell culture , calphostin , cancer research , chemistry , apoptosis , protein kinase c , irradiation , kinase , biochemistry , genetics , physics , nuclear physics
. We assessed the radiosensitivity of the grade III human glioma cell line U‐373MG by investigating the effects of radiation and the specific protein kinase C inhibitor, calphostin C on the cell cycle and cell proliferation. Irradiated glioma U‐373MG cells progressed through G 1 ‐S and underwent an arrest in G 2 ‐M phase. The radiosensitivity of U‐373MG cells to graded doses of either photons or electrons was determine by microculture tetrazolium assay. The data was fitted to the linear‐quadratic model. The proliferation curves demonstrated that U‐373MG cells appear to be highly radiation resistant since 8 Gy was required to achieve 50% cell mortality. Compared to radiation alone, exposure to calphostin C (250 n m ) 1 h prior to radiation decreased the proliferation of U‐373MG by 76% and calphostin C provoked a weakly synergistic effect in concert with radiation. Depending on the time of application following radiation, calphostin C produced an additive or less than additive effect on cell proliferation. We postulate that the enhanced radiosensitivity observed when cells are exposed to calphostin C prior to radiation may be due to direct or indirect inhibition of protein kinase C isozymes required for cell cycle progression.