论文部分内容阅读
背景与目的:肿瘤微环境是影响肿瘤细胞转归的关键因素之一。骨髓微环境能保护白血病细胞,促进白血病细胞耐药、抗凋亡存活,但机制未完全阐明。本研究中我们主要观察骨髓基质细胞促白血病细胞抵抗柔红霉素(daunorubicin,DNR)杀伤的屏蔽效应,旨在探讨骨髓基质细胞增强Jurkat细胞抗凋亡、抗药特性的可能机制。方法:应用Percoll分离正常及白血病性骨髓单个核细胞,体外培养骨髓基质细胞模拟骨髓微环境功能,与白血病细胞Jurkat体外共培养。AnnexinV/PI双标法流式细胞仪检测0.5μmol/LDNR处理后Jurkat细胞凋亡率的变化。PI染色流式细胞仪检测细胞周期分布。结果:共培养后正常骨髓基质细胞抑制DNR诱导的Jurkat细胞凋亡,与单独悬浮培养组比较显著降低[(8.39±4.08)%和(16.02±1.00)%,P<0.05]。白血病骨髓基质细胞对Jurkat细胞的屏蔽效应强于正常骨髓基质细胞[Jurkat细胞凋亡率分别是(5.73±1.78)%和(8.39±4.08)%,P<0.05]。DNR处理正常或白血病骨髓基质细胞共培养组G0/G1期Jurkat细胞比例高于悬浮培养DNR处理组,而正常与白血病骨髓基质细胞屏蔽的Jurkat细胞G0/G1期阻滞现象无显著性差异[(47.96±5.88)%和(39.25±3.04)%,P>0.05]。结论:骨髓基质细胞可能部分通过阻滞白血病细胞于G0/G1期,抑制DNR诱导的白血病细胞?
BACKGROUND & OBJECTIVE: Tumor microenvironment is one of the key factors affecting tumor cell metastasis. Bone marrow microenvironment can protect leukemia cells, promote leukemia cell resistance, anti-apoptotic survival, but the mechanism is not fully elucidated. In this study, we mainly observed the shielding effect of bone marrow stromal cells and leukemia cells against daunorubicin (DNR) killing and aimed to explore the possible mechanism of bone marrow stromal cells enhancing anti-apoptosis and drug resistance of Jurkat cells. Methods: Percoll was used to separate normal and leukemic bone marrow mononuclear cells. BMSCs were cultured in vitro to simulate the microenvironment of bone marrow and co-cultured with leukemic cells Jurkat in vitro. The apoptosis rate of Jurkat cells treated with 0.5μmol / L LDNR was detected by Annexin V / PI double labeling flow cytometry. PI staining flow cytometry to detect cell cycle distribution. Results: Normal bone marrow stromal cells inhibited DNR-induced Jurkat cell apoptosis after co-culture, which was significantly lower than that of the control group [(8.39 ± 4.08)% vs (16.02 ± 1.00)%, P <0.05]. The leukemic bone marrow stromal cells showed stronger shielding effect on Jurkat cells than that of normal bone marrow stromal cells [(5.73 ± 1.78)% and (8.39 ± 4.08)%, respectively, P <0.05]. The proportion of Jurkat cells in G0 / G1 phase of DNR-treated or leukemic BMSCs co-culture group was higher than that in suspension-cultured DNR group, while there was no significant difference in G0 / G1 phase arrest between Jurkat cells and leukemia bone marrow stromal cells [( 47.96 ± 5.88)% and (39.25 ± 3.04)% respectively, P> 0.05]. Conclusion: BMSCs may partially block leukemic cells in G0 / G1 phase and inhibit DNR-induced leukemia cells.