LncRNA NEAT1 promotes colorectal cancer cell proliferation and migration via regulating glial cell-derived neurotrophic factor by sponging miR-196a-5p. (1st November 2018)

• Record Type: Journal Article
• Authors: Zhong, Feng; Zhang, Wei; Cao, Yang; Wen, Qian; Cao, Yue; Lou, Bidan; Li, Jinxiang; Shi, Wenying; Liu, Yinghan; Luo, Rong; Chen, Cheng
• Is Part Of: Acta biochimica et biophysica Sinica. Volume 50:Number 12(2018:Dec.)
• Page Start: 1190
• Page End: 1199
• Publication Date: 2018-11-01
• Subjects: colorectal cancer -- lncRNA -- NEAT1 -- miR-196a-5p -- GDNF; Biochemistry -- Periodicals; Biophysics -- Periodicals; 572.05
• DOI: 10.1093/abbs/gmy130
• Languages: English
• ISSNs: 1672-9145

Abstract

Abstract: Colorectal cancer (CRC) is the one of the most common malignant tumors worldwide. Recent years, widespread long non-coding RNAs (lncRNAs) have been discovered and are known to regulate gene expression in cancers. However, the roles and underlying mechanisms of lncRNA in CRC remain largely unclear. Here, we firstly revealed that repression of lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) inhibited cell proliferation and migration in HCT116 cells and overexpression of NEAT1 promoted cell proliferation and migration in SW480 cells using CCK8 assay and transwell assay. Then, we found that suppression of NEAT1 increased the miR-196a-5p expression in HCT116 cells, while elevation of NEAT1 decreased the miR-196a-5p expression in SW480 cells using qPCR assay. Furthermore, miR-196a-5p could bind to the predicted binding site of NEAT1. We then found that miR-196a-5p was involved in the role of NEAT1 in CRCs. In addition, we demonstrated that miR-196a-5p mimics inhibited the glial cell-derived neurotrophic factor (GDNF) expression in HCT116 cells and meanwhile, miR-196a-5p inhibitor promoted GDNF expression in SW480 cells using qPCR and western blot analysis. Then, we proved that miR-196a-5p exerted its function via regulating GDNF expression in CRCs. Ultimately, our study demonstrated that NEAT1 exerted its role via miR-196a-5p/GDNF axis in CRCs. In summary, this work provided the first evidence of a NEAT1/miR-196a-5p/GDNF regulatory pathway in CRC.