Abstract
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.
Data availability
The authors confirm that all data generated and analyzed during this study are incorporated in the published article and its supplementary information. Data supporting the study findings are available from the corresponding author upon reasonable request, with a commitment to maintaining research integrity and adhering to ethical and confidentiality requirements.
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Acknowledgements
The authors thank the Quanzhou Science & Technology Program and Quanzhou Medical College for funding support. The authors would like to thank all patients for participating in the study.
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This work was supported by: Quanzhou Science & Technology Program (2022N015S).
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Meijie Wu spearheaded manuscript preparation, drafting all sections, conducting initial literature reviews, and ensuring compliance with journal formatting. Yufang Wang enhanced the manuscript through detailed grammatical revisions, improving clarity, and ensuring stylistic and terminological consistency. Guoding He designed the experimental framework, formulating research questions and methodologies, and guiding the study’s scientific direction. Yancheng Lin carried out experimental procedures, including cell culture and data collection, adhering to ethical standards. Ben Liu (Corresponding Author) provided experimental oversight, interpreted results, and coordinated collaborations, ensuring research integrity. Yongzhi Lun oversaw the project, securing funding, and ensuring timely progress. All authors contributed to data interpretation, critically reviewed the manuscript, and approved the final submission, adhering to ethical research standards.
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The collection and use of human lung adenocarcinoma (LUAD) tissue samples were approved by the Ethics Committee of Quanzhou Medical College (Approval No. : 2022011). All experiments involving human tissue samples were conducted in strict accordance with the principles outlined in the Declaration of Helsinki and other relevant ethical guidelines and regulations concerning human subject research.
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Wu, M., Wang, Y., He, G. et al. 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. Sci Rep (2026). https://doi.org/10.1038/s41598-026-39024-2
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DOI: https://doi.org/10.1038/s41598-026-39024-2
