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Long Noncoding RNA SNHG22 Induces Cell Migration, Invasion, and Angiogenesis of Gastric Cancer Cells via microRNA-361-3p/HMGA1/Wnt/β-Catenin Axis

Authors Cui X, Zhang H, Chen T, Yu W, Shen K

Received 15 September 2020

Accepted for publication 19 November 2020

Published 15 December 2020 Volume 2020:12 Pages 12867—12883


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Eileen O'Reilly

Xiaofeng Cui, Huaiyu Zhang, Tong Chen, Wei Yu, Kexin Shen

Department of Gastrointestinal Colorectal and Anal Surgery, China-Japan Union Hospital of Jilin University, Changchun, Jilin 130033, People’s Republic of China

Correspondence: Wei Yu; Kexin Shen
Department of Gastrointestinal Colorectal and Anal Surgery, China-Japan Union Hospital of Jilin University, No. 126, Xiantai Street, Changchun, Jilin 130033, People’s Republic of China
Tel/Fax +86-0431-84996792

Background: The correlation between long non-coding RNAs (lncRNAs) and gastric cancer (GC) has been indicated. As a newly found lncRNA, small nucleolar RNA host gene 22 (SNHG22) functions as an oncogene in ovarian carcinoma and breast cancer. However, its action has not been explored in GC. Herein, the purpose of the current research was to examine the influence of SNHG22 on GC development.
Methods: RT-qPCR was used to identify SNHG22 and microRNA-361-3p (miR-361-3p) in GC tissues and cells. Functional assays were implemented to measure changes on biological activities of GC cells under different transfections. Besides, after human umbilical vein endothelial cells (HUVECs) were co-cultured with supernatant of transfected GC cells, angiogenesis was assessed by tube formation assay in vitro. HMGA1 and β-catenin expression were determined. Finally, mechanistic assays, including RNA pull-down assay and dual-luciferase reporter assay, were employed to assess relationships among SNHG22, miR-361-3p, and HMGA1.
Results: SNHG22 and HMGA1 were highly expressed but miR-361-3p was poorly expressed in GC tissues. Mechanistically, SNHG22 bound to miR-361-3p, and miR-361-3p targeted HMGA1 to disrupt the Wnt/β-catenin pathway. Following SNHG22 or HMGA1 silencing or miR-361-3p upregulation, we observed a decline of proliferation, migration, and invasion of GC cells and HUVEC angiogenesis but acceleration of GC cell apoptosis and cell cycle arrest.
Conclusion: Collectively, SNHG22 silencing possessed tumor-suppressing potentials in GC development via Wnt/β-catenin pathway by binding to miR-361-3p and downregulating HMGA1, highlighting a new promising road for GC treatment development.

Keywords: gastric cancer, long noncoding RNA SNHG22, microRNA-361-3p, HMGA1, Wnt/β-catenin pathway

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