2. Academic Validation
  3. TRPM8 overexpression suppresses hepatocellular carcinoma progression and improves survival by modulating the RTP3/STAT3 pathway

TRPM8 overexpression suppresses hepatocellular carcinoma progression and improves survival by modulating the RTP3/STAT3 pathway

  • Cancer Med. 2024 Oct;13(19):e70109. doi: 10.1002/cam4.70109.
Lichan Chen 1,  Nansong Xu 2,  DongMei Gou 3,  Jianning Song 1,  Mingqin Zhou 4,  Yajun Zhang 5,  Haohua Zhang 1,  Liwen Zhu 1,  Weihong Huang 6,  Yue Zhu 7,  Cheng Gao 1,  Dayong Gu 1,  Yong Xu 3,  Hongzhong Zhou 1
Affiliations

Affiliations

  • 1 Department of Laboratory Medicine, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People's Hospital; Shenzhen Key Laboratory of Medical Laboratory and Molecular Diagnostics; Guangzhou Medical University, Shenzhen, China.
  • 2 State key laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.
  • 3 Shenzhen Third People's Hospital, Southern University of Science and Technology, Shenzhen, China.
  • 4 Department of Critical Care Medicine, Cancer Hospital of Shantou University Medical College, Shantou, China.
  • 5 Guangzhou University of Chinese Medicine, Guangzhou, China.
  • 6 Department of Pathology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.
  • 7 Medicine Department of Biochemistry and Molecular Biology, Medical College of Jinan University, Guangzhou, China.
PMID: 39385506 DOI: 10.1002/cam4.70109
Abstract

Background and aims: Hepatocellular carcinoma (HCC) is a malignant tumour associated with high morbidity and mortality rates worldwide. Recently, TRPM8 was reported to play an important role in tumour progression. However, the precise role of TRPM8 in HCC remains unclear. In this study, we explored the expression levels, molecular functions and underlying mechanisms of TRPM8 in HCC.

Methods: Tissue samples were used to analyse the expression of TRPM8 to assess its diagnostic value for prognosis. Cell Counting Kit-8, EdU and colony formation assays were performed to evaluate the effects of TRPM8 on cell proliferation, whereas the Transwell assay was used to assess cell migration and invasion. The role of TRPM8 in vivo was evaluated using a mouse subcutaneous xenograft tumour model. We performed PPI network analyses to understand the possible mechanisms of TRPM8 action.

Results: TRPM8 expression was decreased in HCC tissues and was correlated with histological grade and poor patient prognosis. Functionally, TRPM8 repressed the proliferation and metastasis of HCC cells both in vitro and in vivo by modulating the RTP3/STAT3 signalling pathway.

Conclusion: Our findings underscore the critical role of the TRPM8-RTP3-STAT3 axis in maintaining the malignant progression of HCC. Moreover, our study demonstrates that AD80 is involved in anti-tumour processes by upregulating the expression of TRPM8.

Keywords

AD80; RTP3/STAT3 pathway; TRPM8; hepatocellular carcinoma.

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