Xiaoxia Liu1, Jihong Wen1, Haijiao Wang1, Yanli Wang2. 1. Department of Gynecology, The First Hospital of Jilin University, Changchun 130021, China. 2. Department of Gynecology, The First Hospital of Jilin University, Changchun 130021, China. Electronic address: wangyl15106@aliyun.com.
Abstract
BACKGROUND: The long non-coding RNA LINC00460 was reported to be involved in the regulation of the malignant phenotype of multiple cancers, and to be a novel diagnostic and therapeutic target. However, its function and mechanisms of action have not yet been fully elucidated in epithelial ovarian cancer (EOC). The aims of this study were to investigate the biological function and underlying mechanism of LINC00460 in EOC progression. MATERIALS AND METHODS: LINC00460 expression was measured in EOC tissues and paired adjacent tissues obtained from 98 patients with EOC by quantitative real time PCR (qRT-PCR). The effect of LINC00460 on cell proliferation, apoptosis, migration and invasion was analyzed by CCK8 assay, flow cytometry, wound healing assay, and Matrigel invasion assay, respectively. Targeting miRNAs of LINC00460 in EOC cells was determined by luciferase reporter assay and qRT-PCR. Protein expression was measured by western blot analysis. RESULTS: LINC00460 expression was upregulated in EOC tissues compared with that in paired adjacent tissues, and higher LINC00460 levels were correlated with advanced International Federation of Gynecology and Obstetrics (FIGO) stage, lymph node metastasis, and shorter overall survival in EOC patients. Knockdown of LINC00460 significantly suppressed cell proliferation, migration, and invasion, and induced apoptosis in EOC cells. A rescue experiment and luciferase reporter assay showed that LINC00460 exerted its oncogenic functions in EOC, at least in part, through binding miR-338-3p. CONCLUSION: LINC00460 may play a crucial role in EOC progression, and may be a promising therapeutic strategy against EOC.
BACKGROUND: The long non-coding RNA LINC00460 was reported to be involved in the regulation of the malignant phenotype of multiple cancers, and to be a novel diagnostic and therapeutic target. However, its function and mechanisms of action have not yet been fully elucidated in epithelial ovarian cancer (EOC). The aims of this study were to investigate the biological function and underlying mechanism of LINC00460 in EOC progression. MATERIALS AND METHODS: LINC00460 expression was measured in EOC tissues and paired adjacent tissues obtained from 98 patients with EOC by quantitative real time PCR (qRT-PCR). The effect of LINC00460 on cell proliferation, apoptosis, migration and invasion was analyzed by CCK8 assay, flow cytometry, wound healing assay, and Matrigel invasion assay, respectively. Targeting miRNAs of LINC00460 in EOC cells was determined by luciferase reporter assay and qRT-PCR. Protein expression was measured by western blot analysis. RESULTS: LINC00460 expression was upregulated in EOC tissues compared with that in paired adjacent tissues, and higher LINC00460 levels were correlated with advanced International Federation of Gynecology and Obstetrics (FIGO) stage, lymph node metastasis, and shorter overall survival in EOC patients. Knockdown of LINC00460 significantly suppressed cell proliferation, migration, and invasion, and induced apoptosis in EOC cells. A rescue experiment and luciferase reporter assay showed that LINC00460 exerted its oncogenic functions in EOC, at least in part, through binding miR-338-3p. CONCLUSION: LINC00460 may play a crucial role in EOC progression, and may be a promising therapeutic strategy against EOC.