CD168 对口腔鳞状细胞癌增殖、 侵袭的作用机制研究

目的 探究 CD168 对口腔鳞状细胞癌增殖、 侵袭的作用机制。 方法 比较人正常口腔角质细胞 系 HOK 与不同口腔鳞癌细胞株间 CD168 表达差异, 选择 HN13 细胞株作为研究对象, 感染慢病毒 shRNA 载体后, 实时荧光定量 PCR (RT-qPCR) 和 Western 印迹法检测 CD168 基因和蛋白表达检测干预效果, CCK-8 法检测细胞增殖情况, 流式细胞仪检测细胞凋亡率, Transwell 试验检测细胞侵袭情况, Western 印迹 检测细胞增殖、 凋亡、 侵袭以及 CXCL12-CXCR4 / CXCR7 信号轴相关蛋白表达。 结果 选择 HN13 细胞和 CD168-shRNA2 慢病毒载体进行后续实验 (P< 0. 05); 沉默 CD168 可使 HN13 细胞增殖、 侵袭数量减少, 细胞凋亡率升高 (P< 0. 05), VEGF、 PCNA、 MMP-2、 MMP-9、 CXCL12、 CXCR4、 CXCR7 蛋白表达量降低 (P< 0. 05), Bax / Bcl-2 比值升高 (P< 0. 05), shRNA-NC 组变化无统计学意义 (P> 0. 05)。 结论 靶向沉 默 CD168 可抑制口腔鳞状癌细胞 HN13 增殖、 侵袭, 促进其凋亡, 可能与 CXCL12-CXCR4 / CXCR7 信号轴 有关。

Effect of CD168 on Proliferation and Invasion of Oral Squamous Cell Carcinoma and Its Mechanism

Objective To explore the effect of CD168 on the proliferation and invasion of oral squamous cell carcinoma and its underlying mechanism. Methods The expression level of CD168 in the human normal oral keratinocyte cell line HOK and several oral squamous cell carcinoma cell lines was compared, and HN13 cell line was selected for the follow-up researches. Gene and protein expression levels of CD168 in cells infected with CD168 shRNA lentivirus were detected by using RT-qPCR and Western blotting. CCK-8 method was applied for the assay of the cell proliferation, the flow cytometry was used for the assay of cell apoptosis and the transwell assay was adopted to detect the cell invasion. Western blotting was performed to detect the expression levels of proteins related to cell proliferation, apoptosis, invasion and CXCL12-CXCR4 / CXCR7 signaling axis. Results The HN13 control cell line and the CD168-shRNA2 cell line were used for further studies (P < 0. 05). Silencing CD168 could suppress the proliferation and invasion of HN13 cells and increase its apoptosis rate (P< 0. 05). The protein expression levels of VEGF, PCNA, MMP-2, MMP-9, CXCL12, CXCR4 and CXCR7 were decreased in the shCH168 cells (P< 0. 05), while the Bax / Bcl-2 ratio was increased ( P < 0. 05), with no statistical changes observed between the shRNA-NC group and the control group (P > 0. 05). Conclusion Silencing of CD168 can inhibit the proliferation and invasion of oral squamous cell carcinoma cell line HN13, and promote their apoptosis, the mechanism may be related to the CXCL12-CXCR4 / CXCR7 signaling axis.