title: In vitro study on apoptosis induced by strontium-89 in human breast carcinoma cell line.
abstract: Many radiopharmaceuticals used for medical diagnosis and therapy are beta emitters; however, the mechanism of the cell death caused by beta-irradiation is not well understood. The objective of this study was to investigate the apoptosis of human breast carcinoma MCF-7 cell lines induced by Strontium-89 (⁸⁹Sr) and its regulation and control mechanism. High-metastatic Breast Carcinoma MCF-7 cells were cultured in vitro using ⁸⁹Sr with different radioactive concentration. The inhibition rate of cell proliferation was measured by MTT color matching method. The cell cycle retardation, apoptosis conditions, mitochondrion transmembrane potential difference and Fas expression were tested and analyzed. The genes P53 and bcl-2 expressions was also analyzed using immunity histochemical analysis. After being induced by ⁸⁹Sr with various of radioactive concentration, it was found that the inhibition of cell proliferation of MCF-7 cells was obviously, the retardation of cell cycle occurred mainly in G2-M. It was also found that the obvious apoptosis occurred after being induced by ⁸⁹Sr, the highest apoptosis rate reached 46.28%. The expressions of Fas acceptor and P53 gene increased, while bcl-2 gene expression decreasesd. These findings demonstrate that in the ranges of a certain radioactive concentration, the inhibition rate of MCF-7 cell proliferation and retardation of cell cycle had positive correlation with the concentration of ⁸⁹Sr. And the mitochondrion transmembrane potential decrease would induce the apoptosis of MCF-7 cell notably, which were controlled by P53 and bcl-2 genes, involved with the Fas acceptor.
authors.affiliation: Department of Nuclear Medicine, Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang 310009, China.
authors.forename: Cheng
authors.initials: C
authors.lastname: Wang
authors.forename: Jing
authors.initials: J
authors.lastname: Wang
authors.forename: Han
authors.initials: H
authors.lastname: Jiang
authors.forename: Min
authors.initials: M
authors.lastname: Zhu
authors.forename: Baoguo
authors.initials: B
authors.lastname: Chen
authors.forename: Weiguang
authors.initials: W
authors.lastname: Bao
mesh_terms: D017209:Apoptosis / Q000528:radiation effects*; D001943:Breast Neoplasms / Q000532:radiotherapy*; D002277:Carcinoma / Q000532:radiotherapy*; D002453:Cell Cycle / Q000528:radiation effects; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000528:radiation effects*; D004307:Dose-Response Relationship, Radiation; D005260:Female; D020869:Gene Expression Profiling; D006801:Humans; D008564:Membrane Potentials / Q000528:radiation effects; D008928:Mitochondria / Q000528:radiation effects; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D019275:Radiopharmaceuticals / Q000627:therapeutic use*; D013326:Strontium Radioisotopes / Q000627:therapeutic use*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D019014:fas Receptor / Q000378:metabolism
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2; D019275:Radiopharmaceuticals; D013326:Strontium Radioisotopes; D016159:Tumor Suppressor Protein p53; D019014:fas Receptor