Long Non‐Coding RNA PTPRG‐AS1 Promotes Proliferation, Migration, and Invasion of Non‐Small Cell Lung Cancer Cells via Modulation of the IGF1/PI3K/AKT Signaling Pathway

Lung cancer is a leading cause of cancer mortality, with non‐small cell lung cancer (NSCLC) comprising the majority of cases. This study aims to investigate the functional role of long non‐coding RNA (lncRNA) PTPRG antisense RNA 1 (PTPRG‐AS1) in NSCLC progression using in vitro models, focusing on its potential as a regulator of key oncogenic processes and its interaction with the IGF‐1/PI3K/AKT signaling pathway to identify novel therapeutic targets. PTPRG‐AS1 expression in NSCLC cell lines (A549, H1299, NCI‐H226) and normal lung cells (Beas‐2B) was analyzed using RT‐qPCR. PTPRG‐AS1 was silenced with siRNA, and its effects on cell proliferation, migration, invasion, colony formation, apoptosis, and angiogenesis‐related factors were evaluated. Western blot analysis assessed components of the PI3K/AKT pathway. LncRNA PTPRG‐AS1 was significantly upregulated in NSCLC cells, particularly in H1299. Our results showed that PTPRG‐AS1 knockdown inhibited cell proliferation, migration, and invasion, while promoting cell apoptosis. IGF‐1 treatment reversed these effects. PTPRG‐AS1 knockdown reduced levels of angiogenesis‐related factors, including VEGF and bFGF. Additionally, silencing PTPRG‐AS1 decreased expression of key PI3K/AKT pathway components, while exogenous IGF‐1 reactivated this signaling cascade. PTPRG‐AS1 plays a critical role in NSCLC progression by modulating the IGF‐1/PI3K/AKT signaling pathway. Targeting PTPRG‐AS1 offers a promising therapeutic strategy for NSCLC, warranting further investigation into its clinical implications.