ArticleBiochemistry and biophysics reports2026
ARHGAP12 loss promotes tumor budding and lymphatic metastasis in gastric cancer.
Article in Biochemistry and biophysics 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.
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Abstract
Background: Identifying the molecular drivers of metastasis and tumor budding (Tb) is essential for improving patient outcomes. This study aimed to characterize the expression pattern and functional contribution of ARHGAP12, a Rho GTPase-activating protein, in the metastatic evolution of GC. Methods: ARHGAP12 expression profiles were analyzed using TCGA_STAD and scRNA-seq (GSE163558) datasets. The spatial distribution of ARHGAP12 in Tb regions and paired lymph node metastases was validated via mIHC in a cohort of 27 GC patients. A highly metastatic cell subline (HGC-27-L) was established through in vivo selection. Functional impacts of ARHGAP12 were evaluated using siRNA knockdown, lentiviral overexpression, wound healing, Transwell migration, and transendothelial migration assays. The prognostic value of ARHGAP12 was assessed using Kaplan-Meier survival analysis. Results: Analysis of scRNA-seq and mIHC data revealed that ARHGAP12 expression was significantly diminished in metastatic foci and Tb cells compared to primary tumor cells ( Conclusion: ARHGAP12 serves as a pivotal suppressor of GC metastasis. Its downregulation facilitates the epithelial-mesenchymal transition and enhances the invasive capacity of tumor cells, particularly within the Tb microenvironment.
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