ArticleDiscover oncology2026
Identification and validation of DPP4 in predicting the prognosis of clear cell RCC.
Article in Discover oncology, 2026. 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
2 authors.
Funding
Abstract
Dipeptidyl peptidase-4 (DPP4) has been implicated in tumor progression, yet its role in clear cell renal cell carcinoma (KIRC) remains poorly understood. This study aimed to comprehensively investigate the expression profile, prognostic significance, and functional mechanisms of DPP4 in KIRC through integrated bioinformatics analysis and experimental validation. Bioinformatics tools (GEPIA, UALCAN, Kaplan-Meier Plotter, STRING, Metascape, TIMER, cBioPortal) were employed to analyze DPP4 expression patterns, promoter methylation status, genetic alterations, immune infiltration characteristics, and clinical correlations using TCGA-KIRC datasets. In vitro experimental validation included qPCR, Western blot, CCK-8 proliferation assays, wound healing assays, and Transwell migration/invasion assays in KIRC cell lines (Caki-1, ACHN, 786-O) and normal renal tubular epithelial cells (HK-2) to elucidate DPP4’s functional roles in tumor progression. Bioinformatics analysis revealed significant upregulation of DPP4 in KIRC tissues compared to normal controls (P < 0.001), with elevated expression strongly correlating with advanced pathological stage (P < 0.001) and poorer overall survival (P < 0.001). Epigenetic analysis demonstrated promoter hypermethylation and genetic alterations (2.2% mutation frequency) associated with KIRC progression. Functional enrichment analysis linked DPP4 to immune regulation (particularly TNF signaling pathway) and epithelial-mesenchymal transition (EMT) processes. Immune profiling via TIMER showed positive correlations between DPP4 expression and infiltration of immunosuppressive cells (Tregs, M2 macrophages). Experimental validation confirmed DPP4 overexpression in KIRC cells, while its knockdown significantly inhibited cellular proliferation, migration, and EMT progression, as evidenced by upregulated E-cadherin and downregulated N-cadherin, Vimentin, and SNAIL expression. A prognostic nomogram incorporating DPP4 expression and clinical parameters demonstrated robust predictive accuracy (AUC = 0.640). DPP4 promotes KIRC progression through dual mechanisms involving EMT activation and immune microenvironment modulation, serving as both an independent prognostic biomarker and a potential therapeutic target. This study provides comprehensive multi-omics insights into the oncogenic role of DPP4 in KIRC, effectively bridging computational predictions with experimental validation.
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.