Objective: To investigate the effect of Busulfan on the malignant biological characteristics of multiple myeloma cells and explore the molecular mechanism.
Methods: Multiple myeloma RPMI8226 cells were treated with Busulfan at different concentrations. Cell proliferation activity was detected by MMT assay, and cell apoptosis was detected by flow cytometry with Annexin V/PI double staining. Real-time quantitative PCR was used to detect the mRNA expression of apoptotic regulatory molecules Bax、Bcl-2 and Wnt3a/β-catenin pathway, and Western blot was used to detect the expression changes of Bax, Bcl-2 and Wnt3a/β-catenin pathway protein.
Results: Busulfan inhibited cell proliferation and induced apoptosis of myeloma RPMI8226 cells (P<0.05). After treatment with Busulfan at different concentrations for 48 h, the expression of anti-apoptotic protein Bcl-2 was decreased, the expression of pro-apoptotic protein Bax was up-regulated, and the activation of Wnt3a/β-catenin signaling pathway was inhibited to induce programmed death of RPMI8226 cells (P<0.05).
Conclusion: Busulfan can inhibit the malignant biological characteristics of myeloma RPMI 8226 cells, and its mechanism may be related to regulating the expression of Bcl-2 family proteins and inhibiting the activation of Wnt3a/β-catenin signaling pathway.
题目: 白消安抑制多发性骨髓瘤细胞恶性生物学特性的分子机制.
目的: 探讨白消安对多发性骨髓瘤细胞恶性生物学特性的影响，并探索其分子机制.
方法: 予不同浓度梯度白消安干预多发性骨髓瘤RPMI8226细胞，MTT法检测细胞增殖活力，Annexin V/PI双染法流式细胞术检测细胞凋亡情况，实时荧光定量PCR技术检测凋亡调控分子Bax、Bcl-2及Wnt3a/β-catenin通路信号分子mRNA的表达情况，Western blot技术检测Bax、Bcl-2及Wnt3a/β-catenin通路蛋白的表达改变.
结果: 白消安可明显抑制骨髓瘤RPMI8226细胞细胞增殖活性，并诱导其凋亡（P<0.05）。予不同浓度白消安干预细胞48 h后，可使抗凋亡蛋白Bcl-2表达减低，并上调促凋亡蛋白Bax的表达，同时抑制Wnt3a/β-catenin信号通路激活以诱导RPMI8226细胞发生程序性死亡（P<0.05）.
结论: 白消安可抑制骨髓瘤RPMI8226细胞恶性生物学特性，其作用机制可能与调控Bcl-2家族蛋白表达及抑制Wnt3a/β-catenin信号通路激活有关.
Keywords: Busulfan; malignant biological characteristics; molecular mechanism; multiple myeloma.