L Peng1, Y-H Liu, S Nie, M Gao. 1. Department of Pediatrics, The First Hospital of Jilin University, Changchun City, Jilin Province, China. gaoman2011@hotmail.com.
Abstract
OBJECTIVE: Cholangiocarcinoma (CCA) is one of the tumors with high malignancy of the liver and bile system, whose development and prognosis mechanisms are still not clear. Here, a preliminary illustration was made on the expression and function of long non-coding RNA (lncRNA) CASC2 and the relevant mechanism of its function. PATIENTS AND METHODS: Expression of CASC2 in CCA tissues and cells were examined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell proliferation ability was detected using colony formation and Cell Counting Kit-8 (CCK-8) assays while cell invasion and migration abilities were measured using transwell and Matrigel assays. Using bioinformatic analysis, underlying downstream molecules of CASC2 were predicted and by Dual-Luciferase assay and Western blot. RESULTS: It was found that CASC2 was expressed at a significantly lower level in CCA tissues and cell lines. The overexpression of CASC2 inhibited QBC939 cell proliferation, invasion and migration when the knockdown of CASC2 accelerated HUCCT1 cell growth and metastasis. Besides, miR-18a was identified as a direct target for CASC2, and SOCS5 as target for miR-18a. Moreover, CASC2 functioned as a sponge of miR-18a to promote the SOCS5 expression, then, slowed down the epithelial-to-mesenchymal transition (EMT) progression. CONCLUSIONS: CASC2 was downregulated in CCA tissues and cells. It could inhibit cell proliferation, invasion, migration and EMT via sponging miR-18a/SOCS5 axis. This might provide a novel target for CCA diagnosis and treatment.
OBJECTIVE:Cholangiocarcinoma (CCA) is one of the tumors with high malignancy of the liver and bile system, whose development and prognosis mechanisms are still not clear. Here, a preliminary illustration was made on the expression and function of long non-coding RNA (lncRNA) CASC2 and the relevant mechanism of its function. PATIENTS AND METHODS: Expression of CASC2 in CCA tissues and cells were examined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell proliferation ability was detected using colony formation and Cell Counting Kit-8 (CCK-8) assays while cell invasion and migration abilities were measured using transwell and Matrigel assays. Using bioinformatic analysis, underlying downstream molecules of CASC2 were predicted and by Dual-Luciferase assay and Western blot. RESULTS: It was found that CASC2 was expressed at a significantly lower level in CCA tissues and cell lines. The overexpression of CASC2 inhibited QBC939 cell proliferation, invasion and migration when the knockdown of CASC2 accelerated HUCCT1 cell growth and metastasis. Besides, miR-18a was identified as a direct target for CASC2, and SOCS5 as target for miR-18a. Moreover, CASC2 functioned as a sponge of miR-18a to promote the SOCS5 expression, then, slowed down the epithelial-to-mesenchymal transition (EMT) progression. CONCLUSIONS:CASC2 was downregulated in CCA tissues and cells. It could inhibit cell proliferation, invasion, migration and EMT via sponging miR-18a/SOCS5 axis. This might provide a novel target for CCA diagnosis and treatment.