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GPR37 promotes the malignancy of lung adenocarcinoma via TGF-β/Smad pathway

Authors
  • Wang, Jian1
  • Xu, Min2
  • Li, Dan-Dan3
  • Abudukelimu, Wujikenayi1
  • Zhou, Xiu-Hong1
  • 1 Department of Respiration, Midong Branch of People’s Hospital of Xinjiang Autonomous Region, 1302-17 Midong South Road, Xinjiang , (China)
  • 2 Department of Medical, Midong Branch of People’s Hospital of Xinjiang Autonomous Region, Xinjiang , (China)
  • 3 Department of Endocrinology, Midong Branch of People’s Hospital of Xinjiang Autonomous Region, Xinjiang , (China)
Type
Published Article
Journal
Open Medicine
Publisher
De Gruyter
Publication Date
Dec 05, 2020
Volume
16
Issue
1
Pages
24–32
Identifiers
DOI: 10.1515/med-2021-0011
Source
De Gruyter
Keywords
License
Green

Abstract

This paper aimed to research the function and in-depth mechanism of GPR37 in lung adenocarcinoma (LUAD). Herein, based on TCGA and Oncomine databases, we revealed that GPR37 was expressed at high levels in LUAD, and upregulation of GPR37 was related to the poor outcomes. Furthermore, biological function experiments in vitro were utilized to assess whether GPR37 impacts malignant phenotype of LUAD cells. Gain- or loss-of-function assays indicated that the upregulation of GPR37 contributed to improving the proliferation, migration, and invasion of LUAD cells in vitro, while knockdown of GPR37 can inhibit the malignant biological behaviors. Then, we found that depletion of GPR37 resulted in a decrease in the expression of TGF-β1 as well as the extents of Smad2 and Smad3 phosphorylation, while overexpression of GPR37 presented opposite outcomes. Altogether, our findings indicated that GPR37 is a potential oncogene of LUAD, and its promoting effects on the malignant progression of LUAD may be realized via TGF-β/Smad pathway.

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