Progression of Non-Small-Cell Lung Carcinoma is Aggravated by LINC01410-Induced Upregulation of PGK1 via the Sponge Effect on miR-4523

Abstract

This study investigates the role of LINC01410 in non-small-cell lung carcinoma (NSCLC) progression and the underlying mechanisms. Differential expressions of LINC01410, miR-4523, and PGK1 were examined in NSCLC and normal specimens using qRT-PCR. Prognostic and diagnostic potentials of LINC01410 were assessed via Kaplan-Meier and ROC analyses. Proliferation and migration rates in LINC01410-manipulated A549 and H1299 cells were evaluated using CCK-8 and transwell assays. Binding relationships between LINC01410/miR-4523 and miR-4523/PGK1 were determined through luciferase assays and correlation tests. Rescue experiments were conducted to elucidate the LINC01410/miR-4523/PGK1 axis’s role in NSCLC cell behavior regulation. LINC01410 and PGK1 were upregulated in NSCLC specimens, while miR-4523 was downregulated. High LINC01410 levels predicted poor NSCLC prognosis, with diagnostic potential confirmed by ROC curves. LINC01410 overexpression significantly enhanced A549 and H1299 cell proliferation and migration. LINC01410 acted as a miR-4523 sponge, and miR-4523 targeted PGK1. PGK1 overexpression partially attenuated LINC01410-induced NSCLC cell proliferation and migration. In conclusion, LINC01410 drives NSCLC cell proliferation and migration by upregulating PGK1 through miR-4523 sequestration.