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

Open Med (Wars)

Department of Respiration, Midong Branch of People's Hospital of Xinjiang Autonomous Region, 1302-17 Midong South Road, Urumqi, Xinjiang, People's Republic of China.

Published: December 2020

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 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 , 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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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7730288PMC
http://dx.doi.org/10.1515/med-2021-0011DOI Listing

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