Mechanism study of lncRNA SNHG1/miR-340-5p/PTX3 signaling pathway in osimertinib resistance of lung cancer
10.3969/j.issn.1673-4130.2025.14.017
- VernacularTitle:lncRNA SNHG1/miR-340-5p/PTX3信号通路在肺癌奥希替尼耐药中的机制研究
- Author:
Lu ZHANG
1
;
Wenli ZHAO
;
Lingwen HE
;
Chenyu XU
Author Information
1. 东莞东华医院肿瘤内科,广东 东莞 523000
- Keywords:
small nucleolar RNA host gene 1;
microRNA-340-5p;
pentraxin 3;
lung cancer
- From:
International Journal of Laboratory Medicine
2025;46(14):1758-1763
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the mechanism of the long non-coding RNA(lncRNA)small nucleolar RNA host gene 1(SNHG1)/microRNA(miR)-340-5p/pentraxin 3(PTX3)signaling pathway in osimertinib resistance of lung cancer.Methods The expression levels of SNHG1,miR-340-5p and PTX3 in lung cancer tissues,adjacent tissues and osimertinib-sensitive and resistant cell lines were detected by real-time fluores-cence quantitative PCR.SNHG1 was knockdown using siRNA to detect its effects on cell proliferation,apopto-sis and osimertinib sensitivity.The dual-luciferase reporter assay verified the binding relationship between SNHG1 and miR-340-5p,as well as between miR-340-5p and PTX3.Western blotting was used to analyze the expression changes of PTX3 protein.Results SNHG1 was highly expressed in lung cancer tissues and osimer-tinib-resistant cells,while the expression of miR-340-5p was downregulated.SNHG1 inhibits the function of miR-340-5p by directly binding to it and releases the negative regulation of miR-340-5p on PTX3,resulting in the high expression of PTX3 in lung cancer drug-resistant cells.Knockdown of SNHG1 can increase the apop-tosis rate of drug-resistant cells,inhibit the ability of colony formation,and enhance the sensitivity of cells to osimertinib.The miR-340-5p inhibitor upregulated the expression of PTX3 in lung cancer sensitive cells.Con-clusion SNHG1 as competitive endogenous RNA inhibition of miR-340-5p,thus raising PTX3 expression,the drug resistance of lung cancer cells,SNHG1/miR-340-5p/PTX3 shaft may provide potential targets in the treatment of lung cancer drug resistance.
