ArticleFrontiers in immunology2025
Unveiling the immunometabolic landscape of colorectal cancer through PANoptosis-related gene expression.
Article in Frontiers in immunology, 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Colorectal cancer (CRC) development and progression are linked to genetic factors, environmental influences, and dysregulated signaling pathways. Methods: The differentially expressed pan-apoptotic genes (CPAN_DEGs) between CRC and normal colon tissues were screened from bulk RNA-sequencing (RNA-Seq) datasets. The putative biological functions of these CPAN_DEGs were explored through functional enrichment analysis and the protein-protein interaction (PI) network. Unsupervised clustering was used to stratify patients on the basis of CPAN_DEGs, and a prognostic model was constructed using LASSO dimensionality reduction. Based on the CPAN-index score, the patients were divided into the high-risk and low-risk groups, and the survival rates and immunophenotypes were compared. The predictive performance of the CPAN-index model was confirmed in an external validation set. The expression patterns of PANoptosis genes across different cell types in CRC samples, and the distribution of CPAN-index-positive cells within each subpopulation were analyzed using single cell RNA-Seq (scRNA-Seq) datasets. The expression of CDKN2A was confirmed in CRC cell lines, and its functional role was evaluated by gene knockdown. Results: The expression levels of PANoptosis-related genes showed significant heterogeneity across CRC samples, and the highest percentage (87.4%) was that of apoptosis-related genes. The differentially expressed genes (DEGs) between the CRC and normal tissue samples were significantly enriched in pathways related to metabolism and immune regulation. The CPAN-index constructed using 11 CPAN_DEGs effectively distinguished CRC patients in to the high-risk and low-risk groups, and the high-risk group showed an "invasion-metabolism-immunosuppressive" phenotype, along with immune tolerance and non-classical immune escape. The CPAN-index gene CDKN2A was upregulated in the CRC cell lines, and knocking down the CDKN2A gene inhibited their proliferation and promoted apoptosis Conclusions: CDKN2A-mediated PANoptosis signaling network drives CRC progression by reshaping the immune microenvironment and metabolic reprogramming. The CPAN-index provides a new tool for accurate risk stratification of CRC patients, and suggests potential therapeutic strategies targeting the immunometabolism-death interaction network.
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.