纤维蛋白胶凝素-3在非小细胞肺癌中的表达及其生物学功能研究

Recombinant ficolin 3 expression in non-small cell lung cancer and its biological function

目的探讨纤维蛋白胶凝素-3(FCN3)调控非小细胞肺癌细胞A549的潜在机制。方法通过在线软件预测对FCN3进行生物信息学分析,并构建其过表达载体和siRNA干扰体系。采用CCK8法和流式细胞仪检测过表达、敲低FCN3对A549细胞增殖和凋亡的影响。采用实时荧光定量聚合酶链反应检测FCN3对肺腺癌相关基因[染色体盒同源物5(CBX3)、细胞周期依赖激酶抑制剂3(CDKN3)和含杆状病毒凋亡抑制蛋白重复序列蛋白5(BIRC5)]表达的影响。结果过表达FCN3后,A549细胞的凋亡水平升高,增殖水平下降,差异有统计学意义(P<0.05)。敲低FCN3后,A549细胞的凋亡水平下降,增殖水平升高,差异有统计学意义(P<0.05)。过表达FCN3可抑制CBX3、CDKN3和BIRC5 mRNA表达,促进FABP4 mRNA表达;敲低FCN3可促进CBX3、CDKN3和BIRC5 mRNA表达,抑制FABP4 mRNA表达。结论FCN3可以抑制A549细胞增殖,并促进其凋亡。FCN3或可作为非小细胞肺癌的潜在治疗靶点。

Objective To explore the potential mechanism of recombinant ficolin 3(FCN3)in regulating non-small cell lung cancer cell line A549.Methods Bioinformatics analysis of FCN3 was performed using online software,and its overexpression vector and siRNA interference system were constructed.CCK8 assay and flow cytometry were used to detect the effects of overexpression and knockdown of FCN3 on the proliferation and apoptosis of A549 cells.Real-time fluorescent quantitative polymerase chain reaction was used to detect the influence of FCN3 on the expression of lung adenocarcinoma-related genes[Chromobox Homolog 5(CBX3),Cyclin-Dependent Kinase Inhibitor 3(CDKN3)and Baculoviral IAP Repeat-Containing Protein 5(BIRC5)].Results After overexpression of FCN3,the apoptosis level of A549 cells increased,and the proliferation level decreased(P<0.05).After knockdown of FCN3,the apoptosis level of A549 cells decreased,and the proliferation level increased(P<0.05).Overexpression of FCN3 inhibited the expression of CBX3,CDKN3 as well as BIRC5 mRNA,and promoted the expression of FABP4 mRNA;knockdown of FCN3 promoted the expression of CBX3,CDKN3 as well as BIRC5 mRNA,and inhibited the expression of FABP4 mRNA.Conclusion FCN3 can inhibit the proliferation of A549 cells and promote their apoptosis.FCN3 may serve as a potential therapeutic target for non-small cell lung cancer.