MiR-129 Weakens Proliferation of Non-Small Cell Lung Cancer Cells via Targeted Regulation of High-Mobility Group AT-Hook 2

Abstract

This study investigated the role of micro ribonucleic acid (miR)-129 in non-small cell lung cancer (NSCLC) by examining its effects on cell proliferation and apoptosis, as well as its relationship with the high-mobility group AT-hook 2 (HMGA2) target gene. Human NSCLC tissues were collected, and cancerous cells and normal cells were isolated and cultured. In vitro cultured NSCLC cells were transfected with miR-129 mimics or HMGA2-small interfering RNA (siRNA). The expression levels of miR-129 and HMGA2 were measured using quantitative reverse transcription-polymerase chain reaction (qRT-PCR), while cell proliferation was assessed using the cell counting kit-8 (CCK-8) assay. The targeted regulation between miR-129 and HMGA2 was examined using a luciferase reporter assay system, and protein expression was determined by Western blotting (WB). Flow cytometry was utilized to measure the cell apoptosis rate. NSCLC tissues and cells exhibited significantly decreased miR-129 expression and increased HMGA2 expression compared to normal tissues and cells. Transfection with miR-129 mimics and HMGA2-siRNA effectively reduced HMGA2 gene and protein expression in NSCLC cells, leading to decreased proliferation and increased apoptosis. The luciferase reporter assay confirmed targeted regulation between miR-129 and HMGA2. In summary, miR-129 may suppress NSCLC cell proliferation and induce apoptosis by targeting HMGA2 expression.