ArticleCancer cell international2025
Comprehensive analysis reveals CLDN9 is a new biomarker in human cancers and immunotherapeutic target for glioblastoma multiforme.
Article in Cancer cell international, 2025. 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
3 authors.
Funding
Abstract
backgroundClaudin-9 (CLDN9) plays a pivotal role in forming tight junctions and adhesion among epithelial cells. Despite its importance, comprehensive investigations into the role of CLDN9 in various cancers have been lacking.
methodsWe conducted a thorough analysis of CLDN9 across multiple cancer types using omics data and assessed its expression in glioblastoma multiforme (GBM) tissues via immunohistochemistry. To explore the impact of CLDN9 on tumor growth, we employed a subcutaneous GBM animal model. Furthermore, we utilized transwell experiments to evaluate cell migration and invasion capabilities.
resultsOur findings reveal significant variations in CLDN9 expression across different cancers and among molecular and immune subtypes. CLDN9 demonstrates impressive predictive accuracy for certain cancer types and shows strong associations with cancer prognosis. IHC confirmed downregulated CLDN9 expression in GBM tissues, and its expression correlated with clinicopathological parameters of GBM patients. Specifically, in GBM, CLDN9 expression negatively correlated with activated CD8 T cells, activated dendritic cells, plasmacytoid dendritic cells, and type 1 helper cells. Moreover, we observed associations between CLDN9 expression and immunostimulators, immunoinhibitors, and major histocompatibility complex molecules. In vitro experiments indicated that CLDN9 overexpression reduced the migratory and invasive capabilities of GBM cells.
conclusionsOverall, our study provides valuable insights into the role of CLDN9 in various tumors and lays a foundation for more precise and individualized immunotherapy approaches for GBM in the future.
Indexed as
Identifiers
What Socratic 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 Socratic graph.