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机构地区:[1]厦门大学附属中山医院血液科,福建厦门361004
出 处:《中国临床药理学杂志》2012年第3期186-189,共4页The Chinese Journal of Clinical Pharmacology
摘 要:目的观察异硫氰酸苯己酯(PHI)体外抑制骨髓瘤细胞增殖的机制。方法 MTT检测PHI对骨髓瘤细胞株RPMI8226增殖的影响;流式细胞术检测药物处理后细胞周期的变化;实时荧光定量PCR检测PHI对Jag2、发状相关增强子基因(Hes1)及人第10号染色体缺失的磷酸酶及张力蛋白同源的基因(PTEN)表达的影响。结果 PHI可抑制RPMI8226细胞增殖,使细胞滞留于G0/G1期。剂量较大的2个实验组较对照组,Jag2表达量的减少与PTEN表达量的增加具有统计学意义(P<0.05);各实验组较对照组Hes1表达量减少均具统计学意义(P<0.05)。结论 PHI可通过靶向抑制Notch信号,上调抑癌基因PTEN,抑制骨髓瘤细胞株的体外增殖。Objective To study the mechanism of proliferating inhibition of phenylhexyl isothiocyanate(PHI) on myeloma cells and support the drug design for targeted therapy for myeloma.Methods MTT test was used to analyze the proliferating inhibition and cell cycle changes were detected by flow cytometry on RPMI8226 cells treated with PHI.The expressions of Jag2,Hes1 and PTEN in RPMI8226 co-cultured with PHI were tested by real-time quantitative PCR.Results The proliferation of RPMI8226 was inhibited by PHI,which also caused the cell cycle of RPMI8226 arrested in G0/G1 phase.Both the decrease of Jag2 and the increase of PTEN in the two groups treated with higher dose PHI have statistical significance(P0.05) compared with the control group.The decrease of Hes1 has statistical significant differences in all test groups compared with the control group(P0.05).Conclusion PHI causes the proliferating inhibition of myeloma cells in vitro by targeted suppress the Notch signal pathway and up-regulate tumor suppressor gene PTEN.
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