ArticleNature communications2026
DKC1 promotes colorectal cancer progression and therapy resistance by dysregulating sphingolipid biosynthesis.
Article in Nature communications, 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
19 authors.
Funding
Abstract
DKC1, a key coordinator of RNA modification and telomerase activity, has been implicated in colorectal cancer (CRC), yet its role in disease pathogenesis remains incompletely understood. We show that DKC1 drives CRC by promoting cell cycle progression, suppressing apoptosis, conferring stemness and drug resistance. Elevated DKC1 in CRC associates with poor prognosis and WNT-enriched Consensus Molecular Subtype 2 gene signature. Mechanistically, canonical WNT-signaling forms a feedback loop with DKC1, driving its expression and oncogenic activity. Comprehensive transcriptomic and lipidomic analyses reveal perturbed sphingolipid metabolism and abundance of specific very-long-chain fatty acid ceramides. Further, a regulatory axis involving DKC1 and SOX2 drives the expression of SGPP2, a critical sphingolipid metabolism mediator. Importantly, DKC1-mediated sphingolipid dysregulation promotes first-line chemoresistance, and FOLFOX-resistant patient-derived organoids effectively respond to DKC1 and WNT signaling inhibitors. Conclusively, we identify the DKC1/WNT axis as a therapeutic target in therapy-resistant CRC and underscore complex sphingolipids as promising plasma-based biomarkers.
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.