Deliang Yu1, Chi Zhang2. 1. Department of Digestive Surgery, Xijing Hospital of Digestive Diseases, Air Force Medical University, Xi'an, 710032, Shaanxi, China. 2. Department of Internal Medicine No. 2, 4th (Xinyuan) Hospital of Yulin, No. 33, Renmin Middle Road, Yulin, 719000, Shaanxi, China. zhangchi7658000@163.com.
Abstract
BACKGROUND: Gastric carcinoma (GC) is one of the most common malignant tumors. Although increasing studies have indicated that circular RNAs function as ideal biomarkers for multiple cancers, only a few researches elucidated the correlation between circular RNA PTK2 (circPTK2) and human cancers. AIM: To further explore the expression status, biological function, and regulatory mechanism of circPTK2 in GC. METHODS: Bioinformatics analysis and function or mechanism experiments including RT-qPCR, flow cytometry, Western blot, luciferase reporter assay, and xenografts assays were applied to investigate the function of circPTK2 and miR-139-3p. RESULTS: High expression of circPTK2 was presented in GC tissues and cells. The circPTK2 knockdown notably suppressed cell proliferation and promoted cell apoptosis in GC. In mechanism, circPTK2 served as a sponge of miR-139-3p. Inhibition of miR-139-3p could reverse circPTK2 silence-mediated effects on GC cell proliferation and apoptosis. Furthermore, the xenograft tumor model was established to investigate the role of circPTK2 in GC tumor growth. Experimental results delineated that the reduction in tumor growth in response to circPTK2 knockdown was partly recovered by miR-139-3p inhibitor. CONCLUSIONS: CircPTK2 promotes GC development by sponging miR-139-3p, which may function as an effective gene target for managing GC.
BACKGROUND:Gastric carcinoma (GC) is one of the most common malignant tumors. Although increasing studies have indicated that circular RNAs function as ideal biomarkers for multiple cancers, only a few researches elucidated the correlation between circular RNA PTK2 (circPTK2) and humancancers. AIM: To further explore the expression status, biological function, and regulatory mechanism of circPTK2 in GC. METHODS: Bioinformatics analysis and function or mechanism experiments including RT-qPCR, flow cytometry, Western blot, luciferase reporter assay, and xenografts assays were applied to investigate the function of circPTK2 and miR-139-3p. RESULTS: High expression of circPTK2 was presented in GC tissues and cells. The circPTK2 knockdown notably suppressed cell proliferation and promoted cell apoptosis in GC. In mechanism, circPTK2 served as a sponge of miR-139-3p. Inhibition of miR-139-3p could reverse circPTK2 silence-mediated effects on GC cell proliferation and apoptosis. Furthermore, the xenograft tumor model was established to investigate the role of circPTK2 in GC tumor growth. Experimental results delineated that the reduction in tumor growth in response to circPTK2 knockdown was partly recovered by miR-139-3p inhibitor. CONCLUSIONS: CircPTK2 promotes GC development by sponging miR-139-3p, which may function as an effective gene target for managing GC.