Cancer genetics · 2025
Regulator of G-protein signaling 14 (RGS14) promotes cancer growth in hepatocellular carcinoma.
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Ran Yi, Li Liping, Wang Zhihua, Sun Ting, Wen Cong, Zhang Yixin, Wang Shu, Jiang Shishi, Zheng Junjie, Yin Changjun, Zhang Chuankai
Аннотация
BACKGROUND: Hepatocellular carcinoma (HCC) is a major contributor to cancer-related deaths globally. The progression of HCC is influenced by a range of intrinsic and extrinsic factors, necessitating further research into the molecular mechanisms involved. While Regulator of G-protein Signaling 14 (RGS14) has shown emerging roles in cancer biology, its function in HCC remains poorly characterized.
MATERIALS AND METHODS: RGS14 expression and clinical significance were analyzed using TCGA-LIHC, HCCDB, and GEO datasets. Immunofluorescence (IF) staining was employed to validate protein expression. Functional assays, including cell proliferation, migration, invasion, and in vivo xenograft models, were conducted to assess the oncogenic role of RGS14. Bulk-mRNA sequencing was performed using in situ tumor tissues to identify RGS14-regulated pathways.
RESULTS: RGS14 was significantly upregulated in HCC tissues and positively associated with poor patient outcomes. In vitro experiments demonstrated that RGS14 enhanced HCC cell proliferation, migration, and invasion, while in vivo studies confirmed its tumor-promoting effects. Mechanistically, RGS14 activated the extracellular matrix (ECM)-receptor interaction pathway to drive HCC progression.
CONCLUSION: Our findings suggest that RGS14 could serve as a novel prognostic marker and therapeutic target for HCC, contributing to improved treatment strategies.
MATERIALS AND METHODS: RGS14 expression and clinical significance were analyzed using TCGA-LIHC, HCCDB, and GEO datasets. Immunofluorescence (IF) staining was employed to validate protein expression. Functional assays, including cell proliferation, migration, invasion, and in vivo xenograft models, were conducted to assess the oncogenic role of RGS14. Bulk-mRNA sequencing was performed using in situ tumor tissues to identify RGS14-regulated pathways.
RESULTS: RGS14 was significantly upregulated in HCC tissues and positively associated with poor patient outcomes. In vitro experiments demonstrated that RGS14 enhanced HCC cell proliferation, migration, and invasion, while in vivo studies confirmed its tumor-promoting effects. Mechanistically, RGS14 activated the extracellular matrix (ECM)-receptor interaction pathway to drive HCC progression.
CONCLUSION: Our findings suggest that RGS14 could serve as a novel prognostic marker and therapeutic target for HCC, contributing to improved treatment strategies.