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Pathophysiologic mechanism of CMTM5 low expression in multiple myeloma progression



Pathophysiologic mechanism of CMTM5 low expression in multiple myeloma progression



Zhonghua Xue Ye Xue Za Zhi 40(1): 58-62



目的: 探索趋化素样因子超家族成员CMTM5表达对多发性骨髓瘤(MM)细胞增殖活性的影响及其机制。 方法: 去甲基化药物地西他滨处理MM细胞系U266细胞,采用实时荧光定量PCR法检测处理前后U266细胞CMTM5、caspase3、caspase9的表达水平并分析其相关性;pcDNA3.1质粒转染U266细胞使CMTM5过表达后,采用CCK-8法检测细胞增殖活性变化。 结果: ①与对照组相比,U266细胞中CMTM5、caspase3和caspase9的mRNA表达水平与地西他滨呈浓度和时间依赖性,随浓度加大和时间延长表达水平增高更加显著(P值均<0.01);U266细胞中CMTM5表达水平与caspase3(r=0.937)、caspase9(r=0.945)呈正相关(P值均<0.001)。②过表达质粒转染的U266细胞,其CMTM5表达水平为133.10±10.35,较空白对照组(0.63±0.14)和质粒对照组(0.64±0.11)显著增高,差异有统计学意义(P值均<0.001);CMTM5过表达U266细胞组72 h细胞增殖活性为0.89±0.08,较对照组(1.32±0.02,t=5.005,P=0.008)和空载质粒组(1.30±0.03,t=4.700,P=0.009)显著降低,差异有统计学意义。 结论: MM细胞中CMTM5的缺失能够被去甲基化药物地西他滨逆转,其变化水平与caspase3、caspase9呈正相关。过表达CMTM5能够抑制U266细胞增殖。.

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Accession: 066446348

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PMID: 30704230


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