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In Vitro Study on Apoptosis Induced by Strontium-89 in Human Breast Carcinoma Cell Line

机译:锶89诱导人细胞凋亡的体外研究 乳腺癌细胞系

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摘要

Many radiopharmaceuticals used for medical diagnosis and therapyare beta emitters; however, the mechanism of the cell death causedby beta-irradiation is not well understood. The objective of thisstudy was to investigate the apoptosis of human breast carcinomaMCF-7 cell lines induced by Strontium-89 (89Sr) and itsregulation and control mechanism. High-metastatic Breast CarcinomaMCF-7 cells were cultured in vitro using 89Sr withdifferent radioactive concentration. The inhibition rate of cellproliferation was measured by MTT color matching method. The cellcycle retardation, apoptosis conditions, mitochondriontransmembrane potential difference and Fas expression were testedand analyzed. The genes P53 and bcl-2 expressions was alsoanalyzed using immunity histochemical analysis. After beinginduced by 89Sr with various of radioactiveconcentration, it was found that the inhibition of cellproliferation of MCF-7 cells was obviously, the retardation ofcell cycle occurred mainly in G2-M. It was also found that theobvious apoptosis occurred after being induced by 89Sr,the highest apoptosis rate reached 46.28%. The expressions ofFas acceptor and P53 gene increased, while bcl-2 gene expressiondecreasesd. These findings demonstrate that in the ranges of acertain radioactive concentration, the inhibition rate of MCF-7cell proliferation and retardation of cell cycle had positivecorrelation with the concentration of 89Sr. And themitochondrion transmembrane potential decrease would induce theapoptosis of MCF-7 cell notably, which were controlled by P53 andbcl-2 genes, involved with the Fas acceptor.
机译:用于医学诊断和治疗的许多放射性药物是β发射器;然而,由β-辐射引起的细胞死亡的机制尚不清楚。本研究的目的是研究锶89(89Sr)诱导人乳腺癌MCF-7细胞凋亡及其调控机制。高放射性乳腺癌MCF-7细胞在体外用不同放射性浓度的89Sr培养。用MTT比色法测定细胞增殖的抑制率。检测并分析了细胞周期阻滞,凋亡条件,线粒体跨膜电位差和Fas表达。还使用免疫组织化学分析法分析了P53和bcl-2基因的表达。经多种放射性浓度的89Sr诱导后,发现MCF-7细胞的细胞增殖抑制作用明显,细胞周期的延迟主要发生在G2-M上。还发现89Sr诱导后发生明显的凋亡,最高凋亡率为46.28%。 Fas受体和P53基因的表达增加,而bcl-2基因的表达减少。这些发现表明,在一定的放射性浓度范围内,MCF-7细胞的增殖抑制率和细胞周期的延迟与89Sr浓度呈正相关。线粒体跨膜电位的降低将明显诱导MCF-7细胞的凋亡,其受Fas受体参与的P53和bcl-2基因的控制。

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