ArticleCell death & disease2026
S100A14 promotes colorectal cancer progression and anti-PD-1 resistance via UPF1-mediated activation of the non-canonical NF-κB signaling.
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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Resistance to anti-PD-1 immunotherapy remains a critical challenge in colorectal cancer (CRC). However, the functional role of S100A14 in CRC remains controversial regarding its oncogenic status and impact on immunotherapy response. Here, integrating single-cell RNA sequencing and tissue microarray analysis, we definitively identify S100A14 as an oncogenic driver of immunotherapy resistance. High S100A14 expression correlates with poor prognosis and an immunosuppressive "cold" tumor phenotype. Mechanistically, S100A14 directly binds UPF1, a core nonsense-mediated mRNA decay (NMD) factor, promoting its ubiquitination-mediated degradation. This impairs the decay of non-canonical NF-κB transcripts (MAP3K14, NFKB2, RELB), causing constitutive pathway activation and PD-L1 upregulation. In co-culture assays, S100A14-overexpressing cells directly suppressed CD8
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.