2. Academic Validation
  3. GPR56 facilitates hepatocellular carcinoma metastasis by promoting the TGF-β signaling pathway

GPR56 facilitates hepatocellular carcinoma metastasis by promoting the TGF-β signaling pathway

  • Cell Death Dis. 2024 Oct 1;15(10):715. doi: 10.1038/s41419-024-07095-6.
Yiming Luo # 1,  Junli Lu # 1,  Zhen Lei 1,  Dean Rao 1,  Tiantian Wang 1,  Chenan Fu 1,  He Zhu 1,  Zhiwei Zhang 1,  Zhibin Liao 2,  Huifang Liang 3,  Wenjie Huang 4 5
Affiliations

Affiliations

  • 1 Hepatic Surgery Centre, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Hubei Key Laboratory of Hepato-Pancreato-Biliary Diseases, Wuhan, Hubei, 430030, China.
  • 2 Hepatic Surgery Centre, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Hubei Key Laboratory of Hepato-Pancreato-Biliary Diseases, Wuhan, Hubei, 430030, China. zhibliao@hust.edu.cn.
  • 3 Hepatic Surgery Centre, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Hubei Key Laboratory of Hepato-Pancreato-Biliary Diseases, Wuhan, Hubei, 430030, China. lianghuifang1997@126.com.
  • 4 Hepatic Surgery Centre, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Hubei Key Laboratory of Hepato-Pancreato-Biliary Diseases, Wuhan, Hubei, 430030, China. huangwenjie@tjh.tjmu.edu.cn.
  • 5 Clinical Medicine Research Center for Hepatic Surgery of Hubei Province; Key Laboratory of Organ Transplantation, Ministry of Education and Ministry of Public Health, Wuhan, Hubei, 430030, China. huangwenjie@tjh.tjmu.edu.cn.
  • # Contributed equally.
PMID: 39353900 DOI: 10.1038/s41419-024-07095-6
Abstract

The metastasis of hepatocellular carcinoma (HCC) poses a significant threat to the survival of patients. G protein-coupled receptor 56 (GPR56) has garnered extensive attention within malignant tumor research and plays a crucial role in cellular surface signal transmission. Nonetheless, its precise function in HCC remains ambiguous. Our investigation reveals a notable rise in GPR56 expression levels in human HCC cases, with heightened GPR56 levels correlating with unfavorable prognoses. GPR56 regulates TGF-β pathway by interacting with TGFBR1, thereby promoting HCC metastasis. At the same time, GPR56 is subject to regulation by the canonical cascade of TGF-β signaling, thereby establishing a positive feedback loop. Furthermore, the combination application of TGFBR1 inhibitor galunisertib (GAL) and GPR56 inhibitor Dihydromunduletone (DHM), significantly inhibits HCC metastasis. Interventions towards this signaling pathway could offer a promising therapeutic approach to effectively impede the metastasis of GPR56-mediated HCC.

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