Impact of miR-519d on the Biological Activity of Non-Small Cell Lung Cancer Cells and Its Mechanism

Altern Ther Health Med. 2024 Jan;30(1):466-471.

Abstract

Objective: This study aimed to investigate the impact of miR-519d on the biological activity of non-small cell lung cancer (NSCLC) cells and elucidate its underlying mechanism.

Methods: An experimental study design was adopted, and a cell culture-based study was conducted. We obtained non-small cell lung cancer cell lines from the ATCC cell bank and categorized them into three groups: the miR group, the NSCLC group, and the Negative control group. Various methods, including flow cytometry, quantitative real-time polymerase chain reaction (qRT-PCR), Transwell assays, Western blotting, and the Cell Counting Kit-8 (CCK-8) assay, were employed to assess miR-519d expression, apoptosis, proliferation, migration, and nuclear factor-kappa B (NF-KB) p65 protein content, thus exploring the impact of miR-519d on the biological activity of NSCLC cells.

Results: In the miR group, we observed the highest expression level of miR-519d in NSCLC cells. Furthermore, the miR group exhibited the greatest number of apoptotic cells and the highest apoptosis rate (P < .05). Notably, the Transwell assay revealed reduced migration of NSCLC cells in the miR group, while the NSCLC cells in the control group exhibited more migratory activity. The cell counts of NSCLC cells also significantly decreased in the miR group, with migration comparable to the Negative control group (P > .05). Western blot analysis indicated that NF-KB p65 protein expression was highest in the Negative control group but significantly reduced in the miR group (all P < .05).

Conclusions: miR-519d is downregulated in NSCLC cells. Elevating the expression of miR-519d inhibits various biological activities of lung cancer cells, including migration and proliferation. The downregulation of NF-KB p65 likely mediates this inhibition.

MeSH terms

  • Carcinoma, Non-Small-Cell Lung* / genetics
  • Cell Proliferation
  • Humans
  • Lung Neoplasms* / genetics
  • MicroRNAs* / genetics
  • MicroRNAs* / metabolism
  • NF-kappa B

Substances

  • MicroRNAs
  • NF-kappa B