Background
Non-small cell lung cancer (NSCLC) is associated with a high mortality and morbidity rate. MicroRNAs participate in tumorigenesis, progression and metastasis of NSCLC. However, miR-6884-5p has not been previously studied. This study aimed to investigate the role of miR-6884-5p in NSCLC and explore its underlying mechanisms.
Conclusions
Our findings demonstrate that miR-6884-5p can inhibit NSCLC cell proliferation, migration, and invasion, suggesting its potential as a therapeutic target for NSCLC treatment.
Methods
We used miR-6884-5p mimics and inhibitors to assess its effects in NSCLC. miR-6884-5p expression levels in NSCLC cell lines were quantified using qRT-PCR. Cell viability was determined using a cell-counting kit 8 assay. Western blot analysis was employed to measure apoptotic proteins. The impact of miR-6884-5p on cell proliferation was assessed via colony formation assay. Furthermore, Transwell assays were utilized to visualize and quantify the effects of miR-6884-5p on NSCLC migration and invasion.
Results
miR-6884-5p mimic significantly inhibited NSCLC cell proliferation to 71.21 % and 72.26 % of control at 5 days of culture time in H460 and HC9 cells (both p < 0.01), respectively, while miR-6884-5p inhibitor significantly promoted cell proliferation to 119.66 % and 126.44 % of control at 5 days of culture time in H460 and HC9 cells (both p < 0.05), respectively. In addition, miR-6884-5p promoted apoptosis by reducing the anti-apoptotic protein B-cell lymphoma 2 (BCL2) protein and increasing apoptotic protein BCL2 associated X protein (all p < 0.01 at least). Moreover, miR-6884-5p effectively suppressed transforming growth factor β1-induced epithelial-mesenchymal transition, as evidenced by the restored expression of E-cadherin (p < 0.01), N-cadherin (p < 0.01) and Vimentin (p < 0.05), leading to the inhibition of migration and invasion in NSCLC cell lines. Conclusions: Our findings demonstrate that miR-6884-5p can inhibit NSCLC cell proliferation, migration, and invasion, suggesting its potential as a therapeutic target for NSCLC treatment.