ArticleFrontiers in immunology2026
GCDCA promotes hepatocellular carcinoma progression through S1PR2/PI3K/AKT-mediated polarization of M2-type macrophages.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- VCAN promotes the progression and recurrence of esophageal squamous cell carcinoma by remodeling the tumor microenvironment.Scientific reports · 2026Article
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Authors and funding
13 authors.
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Abstract
Background: Disorders in bile acid metabolism are recognized as crucial mechanisms in the occurrence and development of hepatocellular carcinoma (HCC), a leading cause of cancer-related deaths worldwide. HCC progression is intricately linked to immune regulation within the tumor microenvironment (TME), particularly involving tumor-associated macrophages (TAMs) that modulate proliferation, invasion, and immune escape. Although glycochenodeoxycholic acid (GCDCA), a primary bile acid, is suspected to influence HCC, the specific mechanisms by which it affects the TME to drive cancer progression remain unclear. Methods: This study investigated the role of GCDCA in HCC progression using a combination of approaches. Single-cell sequencing was employed to analyze the TME and identify a highly malignant subpopulation of cancer stem cells (CSCs). In vivo experiments were conducted using a primary liver cancer model to assess the effect of GCDCA intervention on tumor progression and stemness. Mechanistic exploration focused on the role of the S1PR2 receptor, utilizing both macrophage and tumor cell systems to examine the S1PR2/PI3K/AKT signaling pathway and its influence on macrophage polarization. Results: Single-cell sequencing revealed a distinct subpopulation of CSCs with high malignancy within the TME. Conclusion: This study demonstrates that GCDCA drives HCC progression by inducing M2-type macrophage polarization via the S1PR2/PI3K/AKT signaling pathway, which subsequently enhances tumor cell stemness. These findings elucidate a novel mechanism by which bile acids remodel the TME to promote liver cancer, highlighting potential therapeutic targets within this pathway.
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