Analysis of the mechanism and prognostic value of PRKCQ-AS1 in inhibiting the progression of lung adenocarcinoma via regulating the PD-1/PD-L1 pathway.

[UNLABELLED] To investigate the expression profile and biological functions of long non-coding RNA PRKCQ-AS1 in lung adenocarcinoma (LUAD) and to elucidate the underlying mechanism by which PRKCQ-AS1 modulates tumor immune escape through regulation of the PD-1/PD-L1 signaling pathway. The expression levels and clinical significance of PRKCQ-AS1 in LUAD were analyzed using data from The Cancer Genome Atlas (TCGA) database and validated with clinical specimens. A competitive endogenous RNA (ceRNA) regulatory network mediated by PRKCQ-AS1 was constructed, followed by functional enrichment analysis. PRKCQ-AS1 expression was modulated in NCI-H1395 cells via transfection. Cellular malignant phenotypes were assessed using CCK-8, Transwell, and flow cytometry assays. The regulatory effects on PD-1 and PD-L1 expression were confirmed by RT-qPCR and Western blotting. PRKCQ-AS1 was significantly downregulated in LUAD tissues and negatively correlated with advanced TNM stage and poor prognosis. Mechanistic analyses indicated that the ceRNA network involving PRKCQ-AS1 was strongly associated with immune-related pathways. Silencing of PRKCQ-AS1 markedly enhanced proliferation, migration, and invasion of LUAD cells while suppressing apoptosis in vitro. Notably, knockdown of PRKCQ-AS1 led to a significant upregulation of PD-1 and PD-L1 expression, suggesting that PRKCQ-AS1 inhibits immune escape by suppressing the PD-1/PD-L1 signaling axis. PRKCQ-AS1 acts as a potential tumor suppressor in LUAD. Its downregulation not only promotes tumor progression but also facilitates immune escape through dysregulation of the PD-1/PD-L1 pathway. Therefore, PRKCQ-AS1 may serve as a promising biomarker for prognostic evaluation and a potential therapeutic target for immunotherapy in LUAD.

[SUPPLEMENTARY INFORMATION] The online version contains supplementary material available at 10.1038/s41598-026-39024-2.