Limin Zhao1, Xuefei Zhang2, Huannan Guo1, Mingyang Liu1, Liming Wang3. 1. Department of Oncology, General Hospital of Heilongjiang General Administration of Agriculture and Reclamation, Harbin 150088, People's Republic of China. 2. Department of Thoracic Surgery, The Second Hospital of Dalian Medical University, Dalian 116023, People's Republic of China. 3. Department of Thoracic Surgery, The First Affiliated Hospital of China Medical University, Shenyang 110001, People's Republic of China.
Abstract
PURPOSE: The purpose of this study was to investigate the molecular mechanism of LncRNA LOXL1-AS1 in non-small cell lung cancer (NSCLC). METHODS: Lung cancer cell lines (H1299, A549, H520 and H596) and human normal lung epithelial cell line (BEAS-2B) were used in this study. Gene expression was measured by qRT-PCR (quantitative real-time PCR). The bioinformatics databases (miRDB and TargetScan7) were used to predict target genes. Luciferase assay and pull-down assay were processed for verifying the binding sites. CCK8 assay was used for detecting proliferation, and transwell assay was undertaken for migration and invasion. RESULTS: LncRNA LOXL1-AS1 was higher expressed in lung cancer tissues and cells. Moreover, LOXL1-AS1 expression was upregulated in tumor tissues with advanced stages and metastasis. After knocking down LOXL1-AS1, proliferation, invasion and migration of H1299 and A549 cells were inhibited. Interestingly, miR-3128 was negatively regulated by LncRNA LOXL1-AS1, which inhibited the expression of RHOXF2. Rescue assay also confirmed that miR-3128 inhibitor and oeRHOXF2 could rescue the effect of down-regulated LOXL1-AS1 on proliferation, invasion and migration progression. CONCLUSION: LOXL1-AS1 promotes the progression of NSCLC by regulating miR-3128/RHOXF2 axis, which might be a new potential target for the diagnosis and treatment of NSCLC.
PURPOSE: The purpose of this study was to investigate the molecular mechanism of LncRNA LOXL1-AS1 in non-small cell lung cancer (NSCLC). METHODS: Lung cancer cell lines (H1299, A549, H520 and H596) and human normal lung epithelial cell line (BEAS-2B) were used in this study. Gene expression was measured by qRT-PCR (quantitative real-time PCR). The bioinformatics databases (miRDB and TargetScan7) were used to predict target genes. Luciferase assay and pull-down assay were processed for verifying the binding sites. CCK8 assay was used for detecting proliferation, and transwell assay was undertaken for migration and invasion. RESULTS: LncRNA LOXL1-AS1 was higher expressed in lung cancer tissues and cells. Moreover, LOXL1-AS1 expression was upregulated in tumor tissues with advanced stages and metastasis. After knocking down LOXL1-AS1, proliferation, invasion and migration of H1299 and A549 cells were inhibited. Interestingly, miR-3128 was negatively regulated by LncRNA LOXL1-AS1, which inhibited the expression of RHOXF2. Rescue assay also confirmed that miR-3128 inhibitor and oeRHOXF2 could rescue the effect of down-regulated LOXL1-AS1 on proliferation, invasion and migration progression. CONCLUSION: LOXL1-AS1 promotes the progression of NSCLC by regulating miR-3128/RHOXF2 axis, which might be a new potential target for the diagnosis and treatment of NSCLC.
Authors: T Takata; F Tanaka; T Yamada; K Yanagihara; Y Otake; Y Kawano; T Nakagawa; R Miyahara; H Oyanagi; K Inui; H Wada Journal: Int J Cancer Date: 2001 Impact factor: 7.396
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