Upregulation of lncRNA SUMO1P3 promotes proliferation, invasion and drug resistance in gastric cancer through interacting with the CNBP protein.

Abstract

Gastric cancer (GC) is one type of the most common malignancies in the world. In the process of exploring the pathological mechanism of GC and searching for treatment methods, long non-coding RNAs (lncRNAs) display significant participation. Small ubiquitin-like modifier 1 pseudogene 3 (SUMO1P3) is a newly identified lncRNA, of which the biological role and underlying mechanism in GC progression have not been elucidated. Here, through the comparisons between GC patients' tumor and normal tissue samples, as well as normal gastric mucosal and GC cell lines, we confirmed a significant upregulation of SUMO1P3 in GC tissues and cell lines. Meanwhile, significant upregulation of SUMO1P3 was observed in advanced GC patients, and patients with high level of SUMO1P3 displayed a poor survival rate. Next, gain- and loss-of-function experiments were performed in GC cells, and the results exhibited that SUMO1P3 positively regulated proliferation and invasion of GC cells. Then, we constructed drug-resistant GC cell strains and explore the role of SUMO1P3 in the resistance of GC cells to cisplatin (DDP) and 5-fluorouracil (5-Fu). Finally, bioinformatics analysis and RNA pull-down assay demonstrated that SUMO1P3 could directly interact with cellular nucleic acid binding protein (CNBP), thus positively regulating CNBP downstream oncogenes c-myc and cyclin D1 (CCND1). Our findings indicate that SUMO1P3 promotes proliferation, invasion and drug resistance of GC cells by interacting with CNBP, which reveals a potential prognostic biomarker and a novel therapeutic target for GC.