Junlin Chi1, Tonglei Liu1, Chengmin Shi1, Huayou Luo1, Zhizhong Wu1, Binghong Xiong1, Shuang Liu2, Yujian Zeng3. 1. Department of Gastrointestinal Surgery, First Affiliated Hospital of Kunming Medical University, Kunming 650032, China. 2. Department of Ultrasound, First Affiliated Hospital of Kunming Medical University, Kunming 650032, China. Electronic address: shuangliuaa@163.com. 3. Department of Gastrointestinal Surgery, First Affiliated Hospital of Kunming Medical University, Kunming 650032, China. Electronic address: yujianzeng1@163.com.
Abstract
PURPOSE: The aim of this study was to research the function of lncRNA LUCAT1 in gastric cancer. METHODS: Human gastric cancer tissues and paracancer tissues were obtained from 98 patients undergoing surgical resection in our hospital. The human gastric cancer cell lines (HGC27, BGC823, MGC803, SGC7901 and AGS), and normal gastric mucosal cell line GSE1 were used to research the role of lncRNA LUCAT1. ShRNAs specifically targeting lncRNA LUCAT1, miR-134-5p mimic, miR-134-5p inhibitor and their related controls were transfected into cells. Quantitative real-time PCR was used to detect the expression of lncRNA LUCAT1, miR-134-5p and YWHAZ. The cell proliferation of SGC7901 cells was determined by CCK8 kit. Colony formation assay was undertaken. Cell apoptosis assay was processed using the Annexin V-FITC / propidium iodide (annxinV/PI) apoptosis detection kit. Migration and invasion were detected by transwell assay. Tumor xenograft model was conducted to calculate the size and weight of the tumors. Luciferase reporter assay was used to confirm the interactions among lncRNA LUCAT1, miR-134-5p and YWHAZ. RESULTS: LncRNA LUCAT1 was confirmed to be highly expressed in gastric cancer. Patients with high LUCAT1 level displayed short overall survival and disease-free survival periods. LUCAT1 knockdown or miR-134-5p overexpression decreased the proliferation, colony formation, migration and invasion of SGC7901 cells. CONCLUSIONS: LncRNA LUCAT1 could promote proliferation and invasion of gastric cancer by regulating miR-134-5p/YWHAZ axis.
PURPOSE: The aim of this study was to research the function of lncRNA LUCAT1 in gastric cancer. METHODS:Humangastric cancer tissues and paracancer tissues were obtained from 98 patients undergoing surgical resection in our hospital. The humangastric cancer cell lines (HGC27, BGC823, MGC803, SGC7901 and AGS), and normal gastric mucosal cell line GSE1 were used to research the role of lncRNA LUCAT1. ShRNAs specifically targeting lncRNA LUCAT1, miR-134-5p mimic, miR-134-5p inhibitor and their related controls were transfected into cells. Quantitative real-time PCR was used to detect the expression of lncRNA LUCAT1, miR-134-5p and YWHAZ. The cell proliferation of SGC7901 cells was determined by CCK8 kit. Colony formation assay was undertaken. Cell apoptosis assay was processed using the Annexin V-FITC / propidium iodide (annxinV/PI) apoptosis detection kit. Migration and invasion were detected by transwell assay. Tumor xenograft model was conducted to calculate the size and weight of the tumors. Luciferase reporter assay was used to confirm the interactions among lncRNA LUCAT1, miR-134-5p and YWHAZ. RESULTS: LncRNA LUCAT1 was confirmed to be highly expressed in gastric cancer. Patients with high LUCAT1 level displayed short overall survival and disease-free survival periods. LUCAT1 knockdown or miR-134-5p overexpression decreased the proliferation, colony formation, migration and invasion of SGC7901 cells. CONCLUSIONS: LncRNA LUCAT1 could promote proliferation and invasion of gastric cancer by regulating miR-134-5p/YWHAZ axis.