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.