- VernacularTitle: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
- Author:
Zhen BAO
1
;
Yahong QIAO
Author Information
- Publication Type:Research Article
- Keywords:
non-small cell lung cancer;
A549 cells;
FCN3 gene; cell proliferation; apoptosis; therapeutic target - From: Journal of Clinical Medicine in Practice 2024;28(14):18-23
- CountryChina
- Language:Chinese
-
Abstract:
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 ofFCN3 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 ofFCN3 inhibited the expression ofCBX3, CDKN3 as well asBIRC5 mRNA, and promoted the expression ofFABP4 mRNA; knockdown ofFCN3 promoted the expression ofCBX3, CDKN3 as well asBIRC5 mRNA, and inhibited the expression ofFABP4 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.