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本研究探讨肿瘤坏死因子相关凋亡诱导配体TRAIL对人多发性骨髓瘤细胞系RMPI8226的生长抑制作用,对细胞黏附和凋亡的影响及其作用机制。用MTT法检测TRALL对RPMI8226黏附功能和生长的影响;用AnnexinⅤ/PI检测细胞凋亡;流式细胞学检测细胞表面黏附分子的表达;RT-PCR法测定凋亡相关基因表达水平和Western blot法检测凋亡相关蛋白表达。结果表明:TRAIL抑制RPMI8226细胞生长;可诱导RPMI8226细胞凋亡,并伴有抗凋亡基因Mcl-1、XIAP、cFLIP、CARP1、CARP2和Bcl-2mRNA表达水平下降,促凋亡基因Bax mRNA表达水平升高;RPMI8226细胞内的凋亡执行蛋白caspase-3和NF-κB P65(RelA)表达水平随TRAIL浓度的增加而下降。此外,TRAIL明显上调了RPMI8226细胞表面黏附分子CXCR4的表达。结论TRAIL上调人多发性骨髓瘤细胞株RPMI8226细胞表面的黏附分子CXCR4表达水平。TRAIL可诱导人多发性骨髓瘤细胞株RPMI8226凋亡。在一定的浓度范围内,TRAIL对人骨髓瘤细胞株RPMI8226的生长抑制呈时间-剂量依赖性。
This study was aimed to investigate the effects of tumor necrosis factor-related apoptosis-inducing ligand TRAIL on the growth of human multiple myeloma cell line RMPI8226, its effect on cell adhesion and apoptosis and its mechanism. The effect of TRALL on the adhesion function and growth of RPMI8226 was detected by MTT assay. The apoptosis of RPMI8226 cells was detected by AnnexinⅤ / PI. The expression of cell adhesion molecules was detected by flow cytometry. The expression of apoptosis related genes was detected by RT- Apoptosis-related protein expression was detected. The results showed that TRAIL could inhibit the growth of RPMI8226 cells, induce the apoptosis of RPMI8226 cells, and decrease the expressions of anti-apoptotic genes Mcl-1, XIAP, cFLIP, CARP1, CARP2 and Bcl- . The expression of caspase-3 and NF-κB P65 (RelA) in RPMI8226 cells decreased with the increase of TRAIL concentration. In addition, TRAIL significantly up-regulated the expression of CXCR4 on RPMI8226 cell surface. Conclusion TRAIL up-regulates the expression of CXCR4 on the surface of human multi-myeloma RPMI8226 cells. TRAIL induces apoptosis in human multiple myeloma cell line RPMI8226. At a certain concentration range, the growth inhibition of TRAIL on human myeloma cell line RPMI8226 was time-and dose-dependent.