Long non-coding RNAs (lncRNAs) play significant roles in the pathogenesis of various cancers, including lung cancer. In this study, we aimed to investigate the biological function of lncRNA nuclear enriched abundant transcript 1 (NEAT1) in cancer stem cells (CSCs). CSCs have been suggested as the main cause of tumor metastasis, tumor recurrence, and chemotherapy resistance. The copper transporter 1 (CTR1) has been the focus of many recent studies because of its correlation with cisplatin (CDDP) resistance. So far, the mechanism of how NEAT1 regulates CSCs in NSCLC remains unknown. In the current study, lung cancer stem cells were enriched from the parental NSCLC cells. We observed that NEAT1 was up-regulated while copper transporter 1 (CTR1) was down-regulated in the enriched NSCLC cancer stem cells. Knockdown of NEAT1 was able to decrease the CSC-like properties in NSCLC cells, while over-expression of NEAT1 could contribute to the stemness respectively. Meanwhile, appropriate doses of EGCG restrained the stemness triggered by over-expressing NEAT1 via inducing CTR1 expression. Wnt signal pathway and epithelial-to-mesenchymal transition (EMT) process were involved in NEAT1-induced CSCs in NSCLC. These findings may suggest a novel role of NEAT1 for NSCLC treatment.
Keywords: CTR1; EGCG; NEAT1; NSCLC; cancer stem cells.
© 2017 Wiley Periodicals, Inc.