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

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 genesChromobox 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.