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

Abstract

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.

ELK4-mediated lncRNA SNHG22 promotes gastric cancer progression through interacting with EZH2 and regulating miR-200c-3p/Notch1 axis

“…Recently, Shen et. al demonstrated that SNHG22 induces migration, invasion and angiogenesis of gastric cancer cells via miR-361-3p/HMGA1/Wnt axis [ 29 ]. However, the mechanism for high SNHG22 expression remains unknown.…”

HOXA3-Induced Exosomal lncRNA RNF144A-AS1 Promotes Liver Metastasis of Gastric Cancer via Interacting with PUF60 Protein and Sponging miR-361-3p

“…In addition, RNF144A-AS1 binds to miR-361-3p and reduces the expression of the latter. miR-361-2p has low expression in malignant solid tumors such as prostate cancer (51), ovarian cancer (52), GC (53), non-small cell lung cancer (54,55) and has been con rmed as a tumor suppressor. In this study, it was found that miR-361-3p was low expressed in GC tissues and negatively correlated with RNF144A-AS1 expression.…”

The role of long non-coding RNAs in angiogenesis and anti-angiogenic therapy resistance in cancer

“… 67 lncRNA SNHG22 can upregulate HMGA1 through sponge miR-361-3p to activate Wnt/β-catenin pathway, thereby promoting GC progression ( Figure 2 C). 64 1,081 lncRNAs, 127 microRNAs, and 1,983 differentially expressed mRNAs were screened from RNA-seq data of hepatocellular carcinoma (HCC) patients in the TCGA database. More importantly, lncRNA MYLK-AS1/miR-424-5p/E2F7 axis was the only ceRNA regulatory axis negatively correlated with OS.…”