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Life sciences · Journal article
Advanced Science · August 17, 2026
Raises a question worth testing. It does not answer one.
This mechanistic investigation reports that F7, highly expressed in gastric cancer tissues, promotes metastasis through anoikis resistance and immune evasion via ITGA2–FAK–NF-κB and PI3K–AKT signaling, with reduced CD8+ T-cell infiltration. A small-molecule F7 inhibitor (ThonningianinA) suppressed malignant phenotypes in model systems and enhanced anti-PD-1 efficacy, but no clinical efficacy or human data are presented.
Journal article. Gastric cancer tissue samples and cell-based models. Intervention: F7 signaling pathway interrogation; ThonningianinA compound testing.
F7 was highly expressed in tumor tissues and closely associated with lymph node metastasis and poor prognosis F7 expression was associated with reduced CD8+ T-cell infiltration F7 promoted invasion, migration, and anoikis resistance through ITGA2–FAK–NF-κB signaling
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If validated clinically, F7 inhibition could represent a new approach to overcome immune evasion in metastatic gastric cancer. Current evidence is preclinical and does not yet support clinical translation.
Mechanistic study identifying F7 as a driver of gastric cancer metastasis through cell signaling and microenvironment remodeling, with a potential therapeutic compound tested in model systems but no clinical efficacy data reported.
As stated by the source record.
If validated clinically, F7 inhibition could represent a new approach to overcome immune evasion in metastatic gastric cancer. Current evidence is preclinical and does not yet support clinical translation.
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.
ABSTRACT Coagulation factor VII (F7) has been implicated in tumor progression; however, its role in gastric cancer metastasis and immune evasion remains incompletely understood. In this study, we identified F7 as a clinically relevant driver of gastric cancer. F7 was highly expressed in tumor tissues and closely associated with lymph node metastasis, poor prognosis, and reduced CD8 + T‐cell infiltration. Tumor‐derived autocrine F7 interacted with ITGA2 on the cancer cell surface and activated ITGA2‐associated FAK–NF‐κB signaling and promoted invasion, migration, and anoikis resistance. F7 induced PD‐L1 expression in a manner partly dependent on ITGA2‐mediated PI3K–AKT signaling and promoted collagen I deposition in liver metastatic lesions, which was associated with reduced CD8 + T‐cell infiltration. Co‐immunoprecipitation showed that the K1.2 and K1.3 regions of F7 mediated its interaction with the N‐terminal extracellular region of ITGA2. Further investigations identified HNF4A as an upstream transcription factor of F7, with anoikis‐associated stress enhancing HNF4A nuclear accumulation and F7 transcription. Notably, ThonningianinA (THA) was identified as a potential F7‐targeting small molecule that suppressed F7‐associated malignant phenotypes, reduced tumor growth, and enhanced the antitumor efficacy of anti–PD‐1 therapy. These findings support F7 as a potential therapeutic target for metastatic gastric cancer.
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