ArticleFrontiers in oncology2026
GLIS3 drives epithelial-mesenchymal transition and cancer stem-like traits in stomach adenocarcinoma via TGFBR3-Hedgehog signaling.
Article 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
Background: GLIS family zinc finger 3 (GLIS3) is a transcription factor implicated in multiple malignancies, but its role in stomach adenocarcinoma (STAD) and its downstream effector axis remain unclear. We investigated whether GLIS3 coordinates epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC)-like programs in STAD through a signaling cascade. Methods: GLIS3 expression and prognostic associations were analyzed using transcriptomic datasets from The Cancer Genome Atlas, Genotype-Tissue Expression, and Gene Expression Omnibus. GLIS3 protein levels were evaluated by immunohistochemistry in 133 paired STAD tissues. Survival was assessed by Kaplan-Meier analysis together with multivariable regression models. Gain- and loss-of-function studies were performed in AGS and HGC-27 cells to evaluate proliferation, migration, EMT and CSC-like phenotypes. Mechanistic experiments interrogated a GLIS3-transforming growth factor beta receptor 3 (TGFBR3)-Hedgehog axis using ChIP-qPCR, dual-luciferase assays, co-immunoprecipitation, GLI reporter assays, and vismodegib treatment. Tumor growth was assessed in xenograft models. Results: GLIS3 was consistently upregulated in STAD across public datasets and in the clinical cohort (median H-score: 112 vs 39, Conclusions: GLIS3 identifies an aggressive STAD phenotype and engages a TGFBR3-Hedgehog program linked to EMT and CSC-like features. These findings support further evaluation of GLIS3 as a biomarker for risk stratification and provide a rationale for biomarker-guided targeting of the GLIS3-TGFBR3-Hedgehog axis in STAD.
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