ArticleCell death & disease2026
FOXP4 promotes metastatic progression in colorectal cancer through transcriptional activation of BAG3.
Article in Cell death & disease, 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
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metastatic dissemination remains a major cause of mortality in colorectal cancer (CRC), yet the transcriptional basis of epithelial plasticity is not fully understood. Here, we identified Forkhead Box P4 (FOXP4) as a transcription factor associated with CRC progression. Integrated analyses across multiple patient cohorts, together with single-cell transcriptomic data, showed that FOXP4 is preferentially upregulated in malignant epithelial cells and is associated with poor patient survival. FOXP4 depletion impaired malignant phenotypes in vitro and reduced tumor growth, angiogenesis, and liver metastatic burden in vivo. Mechanistically, FOXP4 bound to the promoter region of the co-chaperone BAG3 and regulated its transcription. Consistent with this, BAG3 restoration or silencing partially reversed the phenotypic changes induced by FOXP4 perturbation. These findings suggest that FOXP4 promotes EMT-associated cellular plasticity, at least in part, through BAG3. Together, these results support a FOXP4-BAG3 regulatory axis linked to EMT-related transcriptional programs in CRC. This study provides additional insight into the molecular basis of epithelial plasticity in CRC and supports further investigation of this pathway.
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.