ArticleScientific reports2026
PFDN2 stabilizes PYCR2 to activate Wnt/β-catenin signaling and promote colorectal cancer progression.
Article in Scientific reports, 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
6 authors.
Funding
Abstract
Colorectal cancer (CRC) progression entails coordinated gene dysregulation and rewiring of signaling networks. Here, we investigated whether prefoldin subunit 2 (PFDN2) contributes to CRC progression by stabilizing pyrroline-5-carboxylate reductase 2 (PYCR2) and thereby modulating Wnt/β-catenin signaling. Integrated analyses of TCGA-COAD/READ and other public datasets showed that PFDN2 and PYCR2 are upregulated in CRC, positively correlated, and associated with poorer prognosis. These findings were corroborated in a 30-pair immunohistochemistry (IHC) cohort, and target modulation was confirmed by quantitative real-time PCR and Western blotting. Gain- and loss-of-function studies showed that PFDN2 promotes, whereas its knockdown suppresses, CRC cell proliferation and migration in vitro; in vivo, PFDN2 silencing reduced xenograft growth and Ki-67/β-catenin expression. PYCR2 was likewise elevated in CRC, linked to adverse clinicopathologic features, and enhanced proliferative and migratory phenotypes. Mechanistically, co-immunoprecipitation and immunofluorescence analyses revealed a PFDN2–PYCR2 interaction with predominantly cytoplasmic colocalization. PFDN2 manipulation altered PYCR2 protein but not mRNA levels; cycloheximide chase and MG132 rescue experiments indicated that PFDN2 stabilizes PYCR2 by limiting proteasome-dependent degradation. PFDN2 or PYCR2 depletion reduced TOP/FOPflash reporter activity, nuclear β-catenin accumulation, and expression of canonical Wnt targets, whereas PYCR2 re-expression partially restored these readouts and migratory capacity in PFDN2-silenced cells. Pharmacologic inhibition of canonical Wnt/β-catenin signaling attenuated the pro-proliferative and pro-migratory effects of PFDN2 or PYCR2 overexpression. The PFDN2–PYCR2–Wnt/β-catenin axis appears to be involved in CRC progression, and both proteins may have potential value as prognostic biomarkers and as candidates for further investigation as therapeutic targets.
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.