Radiation-enhanced expression of major histocompatibility complex class I antigen H-2Db in B16 melanoma cells
Hauser, S.H.; Calorini, L.; Wazer, D.E.; Gattoni-Celli, S.
Cancer Research 53(8): 1952-1955
1993
ISSN/ISBN: 0008-5472 PMID: 8467514 Document Number: 421484
Exposure of eukaryotic cells to ionizing radiation induces several cellular responses including DNA repair, arrest of DNA synthesis, and increased synthesis of specific cellular proteins. We derived from the murine melanoma cell line B16-F10 a clonal isolate (M1) that was exposed to a total dose of 5000 cGy in 25 fractions, according to a protocol that reflects the standard for current radiotherapeutic regimens. We measured, by flow cytometry of fluorescence-stained cells, the surface expression of the two major histocompatibility complex class I antigens H-2D-b and H-2K-b in irradiated M1 cells and untreated M1 controls. We found that after 2000 cGy, expression of H-2D-b antigen was enhanced in irradiated cells versus controls. Radiation-induced expression of H-2D-b antigen appeared to be selective, since no up-regulation of the H-2K-b antigen was detectable, and persisted for at least 5 weeks following the last irradiation. Enhanced H-2D-b antigen expression correlated with increased steady-state levels of H-2D-b mRNA in irradiated cells. These results are consistent with the notion that enhanced expression of major histocompatibility complex class I antigens is part of a long-lasting stress response elicited in cells by radiation.