PCAT6 participates in the development of gastric cancer through endogenously competition with microRNA-30

Y. Xu, J.-Y. Sun, Y.-F. Jin, H. Yu

Department of Gastroenterology, Yantai Yuhuangding Hospital, Yantai, China. YH9080@126.com

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• Oncology

OBJECTIVE: To investigate the role of lncRNA PCAT6 in the progression of gastric cancer and its underlying mechanism.

PATIENTS AND METHODS: Expression levels of PCAT6 in 72 gastric cancer tissues and paracancerous tissues were detected by qRT-PCR (Quantitative Real-Time Polymerase Chain Reaction). The correlation between PCAT6 expression and clinical data of gastric cancer patients was analyzed by the chi-square test. After lentivirus transfection of PCAT6 in gastric cancer cells, proliferation, apoptosis, and invasion were detected by CCK-8 (cell counting kit-8), flow cytometry, and transwell assay, respectively. Western blot was utilized to detect protein expressions of apoptosis-related and EMT-related (epithelial-mesenchymal transition) genes in gastric cancer cells. Furthermore, target genes of PCAT6 were predicted via bioinformatics method and verified by luciferase reporter gene assay. The effects of target genes on biological functions of gastric cancer cells were determined as well.

RESULTS: PCAT6 was overexpressed in gastric cancer tissues than those of paracancerous tissues. PCAT6 expression was negatively correlated to prognosis, tumor size, TNM (tumor node metastasis) stage and metastasis of gastric cancer. For in vitro experiments, overexpression of PCAT6 increased proliferation, migration, and invasion, whereas decreased apoptosis of gastric cancer cells. MicroRNA-30 was predicted as the target gene of TCAT6. Furthermore, microRNA-30 was found to bind to TCAT6 via targeting MKRN3. Either microRNA-30 knockdown or PCAT6 overexpression could remarkably promote MKRN3 expression.

CONCLUSIONS: PCAT6 is overexpressed in gastric cancer, which promotes the development of gastric cancer by endogenously competition with microRNA-30 via targeting MKRN3.

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