LINC01526 Promotes Proliferation and Metastasis of Gastric Cancer by Interacting with TARBP2 to Induce GNG7 mRNA Decay

Abstract

Simple SummaryMany long noncoding RNAs play an important role in gastric cancer progression. In this study, we focused on LINC01526. Through expression and functional analyses, we obtained a preliminary understanding of the pro-cancer role of LINC01526 in gastric cancer. Furthermore, RNA pull-down and RNA immunoprecipitation chip assays demonstrated that LINC01526 interacts with TARBP2, an RNA-binding protein controlling mRNA stability. Moreover, TARBP2 could bind and destabilize GNG7 transcripts. Finally, the rescue assay disclosed that LINC01526 promoted gastric cancer progression by interacting with TARBP2, leading to the degradation of GNG7 mRNA.Gastric cancer is the most common malignancy of the human digestive system. Long noncoding RNAs (lncRNAs) influence the occurrence and development of gastric cancer in multiple ways. However, the function and mechanism of LINC01526 in gastric cancer remain unknown. Herein, we investigated the function of LINC01526 with respect to the malignant progression of gastric cancer. We found that LINC01526 was upregulated in gastric cancer cells and tissues. The function experiments in vitro and the Xenograft mouse model in vivo proved that LINC01526 could promote gastric cancer cell proliferation and migration. Furthermore, LINC01526 interacted with TAR (HIV-1) RNA-binding protein 2 (TARBP2) and decreased the mRNA stability of G protein gamma 7 (GNG7) through TARBP2. Finally, the rescue assay showed that downregulating GNG7 partially rescued the cell proliferation inhibited by LINC01526 or TARBP2 silencing. In summary, LINC01526 promoted gastric cancer progression by interacting with TARBP2, which subsequently degraded GNG7 mRNA. This study not only explores the role of LINC01526 in gastric cancer, but also provides a laboratory basis for its use as a new biomarker for diagnosis and therapeutic targets.