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Downregulation of long non-coding RNA TUG1 suppresses tumor growth by promoting ubiquitination of MET in diffuse large B-cell lymphoma.

Authors
  • Cheng, Hai1
  • Yan, Zhiling1
  • Wang, Xue1
  • Cao, Jiang1
  • Chen, Wei1
  • Qi, Kunming1
  • Zhou, Dian1
  • Xia, Jieyun1
  • Qi, Na1
  • Li, Zhenyu1
  • Xu, Kailin2
  • 1 Blood Diseases Institute, Xuzhou Medical University, Department of Hematology, Key Laboratory of Bone Marrow Stem Cell, The Affiliated Hospital of Xuzhou Medical University, 99 West Huaihai Road, Quanshan District, Xuzhou, 221000, Jiangsu, China. , (China)
  • 2 Blood Diseases Institute, Xuzhou Medical University, Department of Hematology, Key Laboratory of Bone Marrow Stem Cell, The Affiliated Hospital of Xuzhou Medical University, 99 West Huaihai Road, Quanshan District, Xuzhou, 221000, Jiangsu, China. [email protected] , (China)
Type
Published Article
Journal
Molecular and Cellular Biochemistry
Publisher
Springer-Verlag
Publication Date
Nov 01, 2019
Volume
461
Issue
1-2
Pages
47–56
Identifiers
DOI: 10.1007/s11010-019-03588-7
PMID: 31338678
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Long non-coding RNAs (lncRNAs) can modulate gene expression through different mechanisms, but the fundamental molecular mechanism between lncRNAs and MET protein in diffuse large B-cell lymphoma (DLBCL) was poorly understood. The expression of lncRNA TUG1 and MET in DLBCL tissues and cell lines was determined by quantitative real-time PCR and western blotting. Cell proliferation, invasion and apoptosis were determined by cell counting kit-8 assay, transwell assay and flow cytometer. The animal xenograft model was established by the injection of DLBCL cells carrying si-TUG1. The expression of TUG1 and MET was upregulated in DLBCL tissues and cells. We demonstrated that MET was altered in the TUG1 knockdown DLBCL cells, and confirmed the interaction between TUG1 and MET by RNA pull-down and RNA immunoprecipitation. Furthermore, knockdown of TUG1 reduced MET protein level by promoting ubiquitination, and suppressed tumor growth in vitro and in vivo. Our findings demonstrated that TUG1 exerted its oncogenic function in DLBCL by inhibiting the ubiquitination and the subsequent degradation of MET. Knockdown of TUG1 through MET downregulation suppressed DLBCL cell proliferation and tumor growth.

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