Yi Zhu1, Yang Xia, Hongyan Niu, Yijiang Chen. 1. Department of Thoracic Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Abstract
BACKGROUND/AIMS: MicroRNAs (miRNAs) are non-coding small RNAs that regulate cell proliferation and functions by interfering with the translation of target mRNAs. Altered expression of miRNA is known to induce various human malignancies, but little is known about the role of miRNAs in esophageal squamous cell carcinoma (ESCC). METHODS: RT-PCR and Western blot were used to examine the expression of miRNAs and candidate genes in 40 pairs of squamous cell carcinoma of human. MiR-16 mimics and inhibitor were transfected in human TE-1 and Eca-109 cells before detecting the cell migration, proliferation, apoptosis and cell cycle. The regulation mechanism was confirmed by luciferase reporter assay. Caspase-3 and 9 were detected by RT-PCR and Western blot. RESULTS: Aberrant increased level of miR-16 was detected in the ESCC tissues compared with the corresponding adjacent tumor tissues. MiR-16 could inhibit cell apoptosis while promote cell proliferation by down-regulating RECK and SOX6 in TE-1 and Eca-109 cell lines through binding the 3'UTR of both RECK and SOX6 mRNA. CONCLUSIONS: Aberrant expression level of miR-16 could suppress cell apoptosis while promote growth by regulating RECK and SOX6 which play important roles in the pathogenesis of ESCC.
BACKGROUND/AIMS: MicroRNAs (miRNAs) are non-coding small RNAs that regulate cell proliferation and functions by interfering with the translation of target mRNAs. Altered expression of miRNA is known to induce various humanmalignancies, but little is known about the role of miRNAs in esophageal squamous cell carcinoma (ESCC). METHODS: RT-PCR and Western blot were used to examine the expression of miRNAs and candidate genes in 40 pairs of squamous cell carcinoma of human. MiR-16 mimics and inhibitor were transfected in human TE-1 and Eca-109 cells before detecting the cell migration, proliferation, apoptosis and cell cycle. The regulation mechanism was confirmed by luciferase reporter assay. Caspase-3 and 9 were detected by RT-PCR and Western blot. RESULTS: Aberrant increased level of miR-16 was detected in the ESCC tissues compared with the corresponding adjacent tumor tissues. MiR-16 could inhibit cell apoptosis while promote cell proliferation by down-regulating RECK and SOX6 in TE-1 and Eca-109 cell lines through binding the 3'UTR of both RECK and SOX6 mRNA. CONCLUSIONS: Aberrant expression level of miR-16 could suppress cell apoptosis while promote growth by regulating RECK and SOX6 which play important roles in the pathogenesis of ESCC.
Authors: Erika Larrea; Carla Sole; Lorea Manterola; Ibai Goicoechea; María Armesto; María Arestin; María M Caffarel; Angela M Araujo; María Araiz; Marta Fernandez-Mercado; Charles H Lawrie Journal: Int J Mol Sci Date: 2016-04-27 Impact factor: 5.923