Rong He1, Fei Hu Zhang2, Ning Shen3. 1. Department of Respiration, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, China. Electronic address: cbdoctor2@126.com. 2. Department of Emergency, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, China. 3. Department of Respiration, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, China.
Abstract
OBJECTIVE: Recent discoveries verify that long non-coding RNAs (lncRNAs) are important functional regulators involved in non-small cell lung cancer (NSCLC) progression. However, long non-coding RNA FEZF1-AS1 was not been investigated in NSCLC so for. METHODS: We applied the quantitative real time polymerase chain reaction (qRT-PCR) assays to detect the expression of lncRNA FEZF1-AS1 in NSCLC tissues and adjacent normal tissues. Cell proliferation and invasion capacities were evaluated by MTT, colony formation, and cell invasion assays. Chromatin immunoprecipitation (ChIP) and RNA immunoprecipitation (RIP) methods demonstrated the association between lncRNA FEZF1-AS1 expression and E-cadherin. The relative protein expression levels were analyzed by western blot analysis. RESULTS: LncRNA FEZF1-AS1 was significantly up-regulated in NSCLC tissues compared with adjacent normal tissues. Higher lncRNA FEZF1-AS1 expression levels associated with lymph node metastasis, poor differentiation grade and advanced TNM stage. In vitro, we revealed that down-regulation of lncRNA FEZF1-AS1 inhibited cell proliferation and cell invasion capacities in NSCLC. Moreover, down-regulation of lncRNA FEZF1-AS1 suppressed cell epithelial-mesenchymal transition (EMT) process by increasing the expression of E-cadherin and ZO-1, whereas, decreasing the expression of Slug, Twist and Vimentin in NSCLC cells. Furthermore, we demonstrated lncRNA FEZF1-AS1 could epigenetically repress the expression of E-cadherin via binding with LSD1 and EZH2 in NSCLC cells. We also revealed that knockdown of lncRNA FEZF1-AS1 suppressed Wnt/β-catenin signaling in NSCLC. CONCLUSION: These results demonstrated that lncRNA FEZF1-AS1 could function as a tumor promoting regulator in NSCLC, which may provide a target of treatment in NSCLC.
OBJECTIVE: Recent discoveries verify that long non-coding RNAs (lncRNAs) are important functional regulators involved in non-small cell lung cancer (NSCLC) progression. However, long non-coding RNA FEZF1-AS1 was not been investigated in NSCLC so for. METHODS: We applied the quantitative real time polymerase chain reaction (qRT-PCR) assays to detect the expression of lncRNA FEZF1-AS1 in NSCLC tissues and adjacent normal tissues. Cell proliferation and invasion capacities were evaluated by MTT, colony formation, and cell invasion assays. Chromatin immunoprecipitation (ChIP) and RNA immunoprecipitation (RIP) methods demonstrated the association between lncRNA FEZF1-AS1 expression and E-cadherin. The relative protein expression levels were analyzed by western blot analysis. RESULTS: LncRNA FEZF1-AS1 was significantly up-regulated in NSCLC tissues compared with adjacent normal tissues. Higher lncRNA FEZF1-AS1 expression levels associated with lymph node metastasis, poor differentiation grade and advanced TNM stage. In vitro, we revealed that down-regulation of lncRNA FEZF1-AS1 inhibited cell proliferation and cell invasion capacities in NSCLC. Moreover, down-regulation of lncRNA FEZF1-AS1 suppressed cell epithelial-mesenchymal transition (EMT) process by increasing the expression of E-cadherin and ZO-1, whereas, decreasing the expression of Slug, Twist and Vimentin in NSCLC cells. Furthermore, we demonstrated lncRNA FEZF1-AS1 could epigenetically repress the expression of E-cadherin via binding with LSD1 and EZH2 in NSCLC cells. We also revealed that knockdown of lncRNA FEZF1-AS1 suppressed Wnt/β-catenin signaling in NSCLC. CONCLUSION: These results demonstrated that lncRNA FEZF1-AS1 could function as a tumor promoting regulator in NSCLC, which may provide a target of treatment in NSCLC.