Evidence map›Paper›PMID 39385506›Full record

ArticleCancer medicine2024

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

Lichan Chen, Nansong Xu, DongMei Gou, Jianning Song, Mingqin Zhou, Yajun Zhang, Haohua Zhang, Liwen Zhu, Weihong Huang, Yue Zhu and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Lichan ChenDepartment 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.
Nansong XuState key laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.
DongMei GouShenzhen Third People's Hospital, Southern University of Science and Technology, Shenzhen, China.
Jianning SongDepartment 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.
Mingqin ZhouDepartment of Critical Care Medicine, Cancer Hospital of Shantou University Medical College, Shantou, China.
Yajun ZhangGuangzhou University of Chinese Medicine, Guangzhou, China.
Haohua ZhangDepartment 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.
Liwen ZhuDepartment 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.
Weihong HuangDepartment of Pathology, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.
Yue ZhuMedicine Department of Biochemistry and Molecular Biology, Medical College of Jinan University, Guangzhou, China.
Cheng GaoDepartment 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.
Dayong GuDepartment 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.
Yong XuShenzhen Third People's Hospital, Southern University of Science and Technology, Shenzhen, China.ORCID https://orcid.org/0000-0001-6755-6482
Hongzhong ZhouDepartment 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.

Funding

Basic Research General Program of Shenzhen Science and Technology Innovation Commission JCYJ20190809160001751Guangdong Basic and Applied Basic Research Foundation 2020B1111160001Guangdong Basic and Applied Basic Research Foundation 2021A1515110931Guangdong Basic and Applied Basic Research Foundation 2021A1515220084National Key R&D Programmes 2022YFC2302700National Natural Science Foundation of China 82203870Shenzhen Medical Research Funds A2303053Shenzhen Science and Technology Program 201906133000069Shenzhen Science and Technology Program GJHZ20200731095604013Shenzhen Science and Technology Program JCYJ20210324103204011Shenzhen Science and Technology Program JCYJ20210324103407018Shenzhen Science and Technology Program JSGG20220301090003004Shenzhen Science and Technology Program KCXFZ20230731094904008Shenzhen Science and Technology Program RCBS20200714114856016Shenzhen Science and Technology Program SGLH20180625171602058Shenzhen Science and Technology Program ZDSYS20210623092001003Shenzhen Third People's Hospital 23260G1001the Guangdong Science and Technology Foundation 2020A1515110871
6 · The paper itself

Abstract

BACKGROUND AND

aimsHepatocellular 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.

methodsTissue 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.

resultsTRPM8 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.

conclusionOur 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.

Indexed as

Carcinoma, HepatocellularCell ProliferationDisease ProgressionGene Expression Regulation, NeoplasticLiver NeoplasmsSignal TransductionSTAT3 Transcription FactorTRPM Cation ChannelsAnimalsCell Line, TumorCell MovementFemaleHumansMaleMiceMice, NudeSTAT3 protein, humanSTAT3 Transcription FactorTRPM8 protein, humanTRPM Cation ChannelsAD80hepatocellular carcinomaRTP3/STAT3 pathwayTRPM8

Identifiers

PMID39385506
PMCPMC11464657

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