【摘要】 目的:研究过表达集落刺激因子1受体(colony stimulating factor-1 receptor,CSF-1R)对人鼻咽癌(nasopharyngeal carcinoma,NPC)6-10B细胞凋亡的抑制作用及其与Bax和Bcl-2表达之间的关系。方法:体外利用慢病毒构建的CSF-1R过表达载体LV-CSF1R(16957-1)转染到人鼻咽癌6-10B细胞中,实验分转染组和对照组;采用实时荧光定量PCR及Western blotting检测转染后两组细胞中CSF-1R、Bcl-2、Bax的表达情况;CCK-8法检测两组细胞的增殖;流式细胞术检测两组细胞的凋亡情况。结果:转染组的6-10B细胞中其CSF-1 mRNA表达水平明显高于对照组(7.01±0.23 vs 0.09±0.03,P<0.01);Bax mRNA表达水平显著下调(P<0.01),而Bcl-2 mRNA表达水平显著上调(P<0.01)。转染组的6-10B细胞中CSF-1蛋白表达水平明显高于对照组;Bax蛋白表达水平显著下调,而Bcl-2蛋白表达水平稍上调。与对照组相比,转染组6-10B细胞的增殖活力明显提高(P<0.01);凋亡率显著降低[(10.82±0.75)%vs(17.11±0.46)%,P<0.05]。结论:过表达CSF-1R可以通过调节Bax/Bcl-2之间的比例关系来促进鼻咽癌6-10B细胞的恶性增殖,并抑制细胞凋亡。更多还原

【Abstract】 Objective: To investigate the inhibitory effect of Colony stimulating factor-1 receptor(CSF-1R) on apoptosis of human nasopharyngeal carcinoma 6-10B cells and its relationship with Bax/Bcl-2 expression. Methods: Lentiviral vector over-expressing CSF-1R LV-CSF1 R(16957-1)was constructed and trasfected into 6-10B cells; meanwhile a control group was set; The expression of CSF-1R, Bcl-2 and Bax was detected by Real-time PCR and Western blotting. CCK-8 assay and flow cytometry(FCM) were used to detect the cell proliferation and apoptosis, respectively. Results: The mRNA expression of CSF-1R increased significantly in 6-10B cells of transfection group compared with negative control(NC) group(7.01±0.23 vs 0.09±0.03, P<0.01); The expression of Bax mRNA was significantly down-regulated while the expression of Bcl-2 mRNA was significantly up-regulated in 6-10B cells of transfection group(all P<0.01). The protein expression of CSF-1 in 6-10B cells of transfection group was significantly higher than that of control group, along with the remarkably down-regulated Bax protein expression and slightly up-regulated Bcl-2 protein in transfection group. Compared with NC group, the proliferation vitality of 6-10B cells were extremely increased after transfection(P<0.01); however, the cell apoptosis was significantly reduced([10.82±0.75]% vs [17.11±0.46]%, P<0.05). Conclusion: Over-expression of CSF-1R could promote the malignant growth and inhibit the apoptosis of nasopharyngeal carcinoma 6-10B cells by regulating the ratio of Bax/Bcl-2 expression.更多还原