ReviewFrontiers in oncology2026
Isoform-resolved 14-3-3/YWHA networks in colorectal cancer: phospho-adaptor mechanisms, biomarker contexts and therapeutic opportunities.
Review in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
YWHA/14-3-3 proteins are conserved phosphoserine/phosphothreonine-binding adaptors that coordinate signaling-complex assembly, subcellular localization, stress responses and cell-state transitions. Although often discussed as a single adaptor family, colorectal cancer (CRC) studies suggest that individual YWHA isoforms act through distinct clients, RNA-associated layers and tumor-state contexts. In this narrative and mechanistic review, we synthesized PubMed-indexed CRC literature through 18 May 2026 and appraised CRC-relevant mechanistic modules using an explicit evidence-maturity rubric developed by the authors distinct from formal GRADE assessment. We propose an isoform-client-context framework for interpreting 14-3-3 biology in CRC. YWHAG has been linked to CTTN-dependent Wnt/β-catenin activation, whereas YWHAE/14-3-3ϵ protein has been associated with extracellular-vesicle secretion and EV-associated β-catenin/Wnt outputs. Separately, the YWHAE-encoded lncRNA, hereafter referred to as YWHAE lncRNA, has been proposed to activate KRAS/ERK and PI3K/AKT signaling through a competing endogenous RNA mechanism. YWHAZ participates in epithelial-mesenchymal and G2/M transitions through miR-1-3p- and TRIP13-associated mechanisms. YWHAB supports PIK3R2-dependent PI3K/AKT signaling, whereas YWHAH connects NAT10/ac4C regulation, CD8+ T-cell exhaustion and MAPK/ERK-dependent autophagy-associated invasion. SFN illustrates context-dependent tumor-suppressive or stress-adaptive functions. Overall, total 14-3-3 abundance is insufficient for mechanistic or translational interpretation. Interactomics, phosphoproteomics, spatial profiling, extracellular-vesicle analysis and patient-derived models should be used to prioritize YWHA-dependent candidate mechanisms for functional validation. These modules should currently be regarded as testable biomarker and therapeutic hypotheses, not as clinically validated CRC biomarkers or targets.
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