ArticleDose-response : a publication of International Hormesis Society
Peptidylprolyl Isomerase a Regulates DNA Damage Repair and Serves as a Prognostic Biomarker in Lung Adenocarcinoma.
Article in Dose-response : a publication of International Hormesis Society. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: This study investigated the role of peptidylprolyl isomerase A (PPIA) in lung adenocarcinoma (LUAD) using bioinformatics approaches and experimental validation. Methods: This study began by assessing PPIA expression and its prognostic significance in LUAD. We then performed functional enrichment analyses and examined CNVs, DNA methylation, DNMT activity, RNA modification, immune cell infiltration, and drug therapy efficacy. Cellular experiments were performed to confirm the role of PPIA in DNA damage repair. Results: PPIA was overexpressed in LUAD tissues and was associated with poor prognosis, including shorter overall survival and progression-free interval. PPIA expression was correlated with CNVs, DNA methylation, DNMT activity, and RNA modification-related genes. It was also negatively associated with immune cell infiltration and immune-related gene expression, suggesting a potential immunosuppressive role. Drug sensitivity analysis indicated that PPIA may serve as a predictive biomarker for therapeutic efficacy in LUAD. In addition, PPIA expression was associated with DNA damage repair-related genes. Cellular experiments show that PPIA knockdown increases radiosensitivity and γ-H2AX foci formation, whereas PPIA overexpression exerts the opposite effects. Conclusion: This study highlights the potential of PPIA as a prognostic biomarker and target in LUAD, particularly in the regulation of DNA damage repair and tumor immune microenvironment remodeling.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.