ArticleJournal of cancer research and clinical oncology2025
RGS14 promotes the progression of hepatocellular carcinoma by activating the cAMP/PKA/CREB signaling pathway.
Article in Journal of cancer research and clinical oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- GPCRs in CAR-T Cell Immunotherapy: Expanding the Target Landscape and Enhancing Therapeutic Efficacy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- ENPP2 Dysregulation Defines a Candidate Biomarker Axis Coupling Tumor-Intrinsic cAMP Signaling to Macrophage Polarization in Hepatocellular Carcinoma.Human mutation · 2026Article
- Transcriptomics-based identification of lysine crotonylation-related biomarkers in pre-eclampsia.BMC pregnancy and childbirth · 2025Article
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Abstract
backgroundG protein-coupled receptors (GPCRs) mediate the intracellular signals that drive tumor development. Regulator of G protein signaling 14 (RGS14), a key negative regulator of GPCR signaling, influences liver injury, fat metabolism, and inflammation. However, the role of RGS14 in hepatocellular carcinoma (HCC) progression and its underlying mechanisms remain unclear.
methodsIn this study, we compared three pairs of HCC tissues and matched portal vein tumor thrombus (PVTT) samples using 4D-FastDIA proteomics to identify differentially expressed proteins. The clinical significance of RGS14 expression was further evaluated in HCC patient cohorts. Stable RGS14-overexpressing/knockdown cell models were established for functional assays (CCK-8, colony formation, Transwell, and wound healing assays). Additionally, tumor proliferation was evaluated through in vivo studies using a subcutaneous xenograft mouse model. RNA sequencing and western blot analysis were subsequently applied to validate the potential downstream signaling pathways.
resultsThe results revealed that RGS14 was overexpressed in HCC tissues, which was correlated with adverse clinical outcomes. We also confirmed that RGS14 increased the proliferation, colony formation, migration, and invasion and promoted the epithelial‒mesenchymal transition (EMT) of HCC cells both in vitro and in vivo. Mechanistically, RGS14 elevated intracellular cAMP levels, activating the PKA/CREB axis to drive HCC progression.
conclusionOur findings suggest that RGS14 plays a critical oncogenic role in HCC by regulating cAMP/PKA/CREB pathway activation, underscoring its potential as both a prognostic marker and therapeutic target for HCC patients.
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