Objective: To investigate the expression of miR-29b-3p in tissues and cells of non-small-cell lung cancer (NSCLC) and its effect on cisplatin resistance in NSCLC cells and its mechanism.
Methods: The mRNA expression of miR-29b-3p and COL1A1 in NSCLC tissue, cell line A549 and cisplatin-resistant cell line A549/DDP was detected by RT-qPCR. MiR-29b-3p Mimics was transfected into A549/DDP cells, and the cell viability, proliferation, apoptosis and related protein expression were detected by CCK-8, flow cytometry and Western blot. Also, luciferase reporter gene assay was used to verify the targeting relationship between miR-29b-3p and COL1A1. Moreover, COL1A1 overexpression lentivirus and miR-29b-3p mimics (Mimics+COL1A1) were simultaneously transfected into A549/DDP cells, and then the cell viability and related protein expression were measured.
Results: In NSCLC tissue and its cell line, miR-29b-3p was downregulated and COL1A1 was upregulated (P< 0.05). After A549/DDP cell was transfected by mimics, its cell viability and proliferation rate decreased, apoptosis rate and the expression of tumor suppressor gene PTEN and apoptosis-related protein BAX were increased (P< 0.05), which could be reversed by Mimics+COL1A1 co-transfection. Luciferase reporter gene assay indicated that COL1A1 was the target gene of miR-29b-3p.
Conclusion: All in all, miR-29b-3p can reverse the cisplatin resistance of A549/DDP cells by inhibiting the expression of COL1A1 gene and increasing the expression of PTEN and BAX.
Keywords: MiR-29b-3p, non-small-cell lung cancer, COL1A1, cisplatin, drug resistance