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Digestive System Neoplasms / Therapy Resistance / Drug Resistance, Neoplasm · Journal article
Cancer Biology & Therapy · July 27, 2026
Early or partial results. Treat as a signal, not a conclusion.
This narrative review classifies 14-3-3-client stress-response modules in five digestive cancers on the basis of mechanistic and functional evidence, identifying stress-specific complexes as more clinically relevant units than total 14-3-3 expression. No new primary data or quantified clinical endpoints are presented; the evidence is mechanistic and preclinical in origin.
Narrative review. Patients with gastric, colorectal, pancreatic, hepatocellular and biliary cancers.
In gastric cancer, G3BP1 cooperates with YWHAZ-encoded 14-3-3ζ to retain pro-apoptotic Bax in the cytoplasm In colorectal cancer, SFN-encoded 14-3-3σ restricts Yin Yang 1 (YY1), sustaining unfolded protein response and chemotherapy tolerance In pancreatic cancer, SFN-encoded 14-3-3σ interacts with YAP1 to promote ribonucleotide reductase expression and gemcitabine resistance
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The conceptual framework suggests that therapeutic targeting should focus on stress-specific 14-3-3-client interactions rather than global 14-3-3 inhibition; however, no clinical trial data or patient outcome measures are provided to guide implementation.
Narrative review synthesizing mechanistic evidence from functional studies in digestive cancers; no new primary data, clinical validation limited, and therapeutic translation not yet established.
As stated by the source record.
The conceptual framework suggests that therapeutic targeting should focus on stress-specific 14-3-3-client interactions rather than global 14-3-3 inhibition; however, no clinical trial data or patient outcome measures are provided to guide implementation.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
14-3-3 proteins are phosphoserine- and phosphothreonine-binding adaptors that regulate client localization, stability and activity under cellular stress. This narrative review synthesizes stress-specific 14-3-3-client modules in gastric, colorectal, pancreatic, hepatocellular and biliary cancers. Modules were classified as high, moderate, early/context-dependent or background according to mechanistic evidence, functional perturbation, client mapping, treatment-state validation and clinical association. In gastric cancer, G3BP stress granule assembly factor 1 (G3BP1) cooperates with YWHAZ-encoded 14-3-3ζ to retain pro-apoptotic Bax in the cytoplasm. In colorectal cancer, SFN-encoded 14-3-3σ restricts Yin Yang 1 (YY1), sustaining the unfolded protein response and chemotherapy tolerance. In pancreatic cancer, SFN-encoded 14-3-3σ interacts with Yes-associated protein 1 (YAP1) to promote ribonucleotide reductase expression and gemcitabine resistance. In hepatobiliary cancers, SFN-related modules support anoikis resistance but remain context dependent. Clinically relevant units are stress-specific 14-3-3-client complexes rather than total 14-3-3 expression.
Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.