S-Y Yu1, H Peng, Q Zhu, Y-X Wu, F Wu, C-R Han, B Yan, Q Li, H-G Xiang. 1. Department of General Surgery, and Department of Pathology; Pudong New Area People's Hospital Affiliated with Shanghai University of Medicine & Health Sciences, Shanghai, China. 13817081296@163.com.
Abstract
OBJECTIVE: The current study aimed to examine the role and mechanism of a conserved long noncoding RNA termed NORAD (noncoding RNA activated by DNA damage, also named LINC00657) in gastric cancer (GC) progression. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to determine the expression level of relevant genes in GC cell lines. Cell proliferation was examined by cell counting kit-8 (CCK-8) assays. Cell migration and invasion were detected by transwell migration and invasion assays. Protein levels of the indicated genes were detected by Western blotting. Cell apoptosis was examined by flow cytometry. RESULTS: Results showed that NORAD knockdown decreased cell proliferation, migration and invasion but increased cell apoptosis. NORAD knockdown affected the expression of genes related to apoptosis and Epithelial-Mesenchymal Transition (EMT). In addition, NORAD's depletion resulted in reduced Ras Homolog Family Member A (RhoA) and Rho-associated coiled-coil containing protein kinase 1 (ROCK1) expression. Furthermore, NORAD's expression was positively correlated with RhoA and ROCK1 expressions in GC based on The Cancer Genome Atlas (TCGA) database. CONCLUSIONS: Our results demonstrate the oncogenic role of NORAD in gastric cancer progression.
OBJECTIVE: The current study aimed to examine the role and mechanism of a conserved long noncoding RNA termed NORAD (noncoding RNA activated by DNA damage, also named LINC00657) in gastric cancer (GC) progression. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to determine the expression level of relevant genes in GC cell lines. Cell proliferation was examined by cell counting kit-8 (CCK-8) assays. Cell migration and invasion were detected by transwell migration and invasion assays. Protein levels of the indicated genes were detected by Western blotting. Cell apoptosis was examined by flow cytometry. RESULTS: Results showed that NORAD knockdown decreased cell proliferation, migration and invasion but increased cell apoptosis. NORAD knockdown affected the expression of genes related to apoptosis and Epithelial-Mesenchymal Transition (EMT). In addition, NORAD's depletion resulted in reduced Ras Homolog Family Member A (RhoA) and Rho-associated coiled-coil containing protein kinase 1 (ROCK1) expression. Furthermore, NORAD's expression was positively correlated with RhoA and ROCK1 expressions in GC based on The Cancer Genome Atlas (TCGA) database. CONCLUSIONS: Our results demonstrate the oncogenic role of NORAD in gastric cancer progression.