The cross-talk between DDR1 and STAT3 promotes the development of hepatocellular carcinoma.


Journal

Aging
ISSN: 1945-4589
Titre abrégé: Aging (Albany NY)
Pays: United States
ID NLM: 101508617

Informations de publication

Date de publication:
27 07 2020
Historique:
received: 24 02 2020
accepted: 27 05 2020
pubmed: 28 7 2020
medline: 25 3 2021
entrez: 28 7 2020
Statut: ppublish

Résumé

To investigate the function of discoidin domain receptor 1 (DDR1) in hepatocellular carcinoma (HCC) and to further clarify the underlying mechanism. DDR1 was significantly increased in HCC tissues and cells, which was related to clinical staging and prognosis of HCC. Upregulation of DDR1 promoted EMT and glutamine metabolism in HCC cells, while loss of DDR1 showed the opposite effects. STAT3 bound with the promoter of DDR1, and facilitated the phosphorylation of STAT3. In turn, activation of STAT3 increased the expression of DDR1. Silencing of STAT3 removed the promoting effect of DDR1 on proliferation, migration and invasion of HCC cells. The in vivo tumor growth assay showed that the cross-talk between DDR1 and STAT3 promoted HCC tumorigenesis. Our research revealed the positive feedback of DDR1 and STAT3 promoted EMT and glutamine metabolism in HCC, which provided some experimental basis for clinical treatment or prevention of HCC. The mRNA expression of DDR1 was detected by qRT-PCR. CCK8 assay, wound healing assay and transwell assay were used to detect the DDR1/ STAT3 function on proliferation, migration and invasion in HCC cells. Western blot was used to calculate protein level of DDR1, STAT3, epithelial-mesenchymal transition (EMT) related proteins.

Identifiants

pubmed: 32716315
pii: 103482
doi: 10.18632/aging.103482
pmc: PMC7425490
doi:

Substances chimiques

STAT3 Transcription Factor 0
STAT3 protein, human 0
Glutamine 0RH81L854J
DDR1 protein, human EC 2.7.10.1
Discoidin Domain Receptor 1 EC 2.7.10.1

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

14391-14405

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Auteurs

Ye Lin (Y)

Department of General Surgery, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou,Guangdong Province, China.

Haosheng Jin (H)

Department of General Surgery, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou,Guangdong Province, China.

Xianqiu Wu (X)

State Key Laboratory of Oncology in Southern China, Collaborative Innovation Center for Cancer Medicine, Department of Experimental Research, Sun Yat-Sen University Cancer Center, Guangzhou, Guangdong Province,China.

Zhixiang Jian (Z)

Department of General Surgery, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou,Guangdong Province, China.

Xiongfeng Zou (X)

Department of General Surgery, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou,Guangdong Province, China.

Jianfeng Huang (J)

Department of General Surgery, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou,Guangdong Province, China.

Renguo Guan (R)

Department of General Surgery, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou,Guangdong Province, China.

Xiangling Wei (X)

Department of General Surgery, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou,Guangdong Province, China.

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Classifications MeSH