The miR-19b-3p-MAP2K3-STAT3 feedback loop regulates cell proliferation and invasion in esophageal squamous cell carcinoma.


Journal

Molecular oncology
ISSN: 1878-0261
Titre abrégé: Mol Oncol
Pays: United States
ID NLM: 101308230

Informations de publication

Date de publication:
05 2021
Historique:
revised: 22 01 2021
received: 18 08 2020
accepted: 26 02 2021
pubmed: 5 3 2021
medline: 1 4 2022
entrez: 4 3 2021
Statut: ppublish

Résumé

Esophageal squamous cell carcinoma (ESCC) is one of the most refractory malignancies worldwide. Mitogen-activated protein kinase 3 (MAP2K3) has a contradictory role in tumor progression, and the function and expression patterns of MAP2K3 in ESCC remain to be determined. We found that MAP2K3 expression to be downregulated in ESCC, and MAP2K3 downregulation correlated with clinically poor survival. MAP2K3 inhibited ESCC cell proliferation and invasion in vitro and in vivo. MAP2K3 suppressed STAT3 expression and activation. Mechanistically, MAPSK3 interacted with MDM2 to promote STAT3 degradation via the ubiquitin-proteasome pathway. Furthermore, exosomal miR-19b-3p derived from the plasma of patients with ESCC could suppress MAP2K3 expression to promote ESCC tumorigenesis. STAT3 was found to bind to the MIR19B promoter and increased the expression of miR-19b-3p in ESCC cells. In summary, our results demonstrated that the miR-19b-3p-MAP2K3-STAT3 feedback loop regulates ESCC tumorigenesis and elucidates the potential of therapeutically targeting this pathway in ESCC.

Identifiants

pubmed: 33660414
doi: 10.1002/1878-0261.12934
pmc: PMC8096789
doi:

Substances chimiques

MIRN19 microRNA, human 0
MicroRNAs 0
STAT3 Transcription Factor 0
STAT3 protein, human 0
MAP Kinase Kinase 3 EC 2.7.12.2
MAP2K3 protein, human EC 2.7.12.2

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1566-1583

Informations de copyright

© 2021 The Authors. published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.

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Auteurs

Ying Zhang (Y)

Department of Pathology, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Sun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.

Weiqing Lu (W)

Department of Orthopaedics, First Affiliated Hospital of Shantou University Medical College, Shantou, China.

Yelong Chen (Y)

Department of Orthopaedics, First Affiliated Hospital of Shantou University Medical College, Shantou, China.

Youbin Lin (Y)

Department of Orthopaedics, First Affiliated Hospital of Shantou University Medical College, Shantou, China.

Xia Yang (X)

Sun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.

Hu Wang (H)

Department of Orthopaedics, First Affiliated Hospital of Shantou University Medical College, Shantou, China.

Zhaoyong Liu (Z)

Department of Orthopaedics, First Affiliated Hospital of Shantou University Medical College, Shantou, China.

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Classifications MeSH