Abstract
Background: Cholangiocarcinoma (CCA) is a serious malignant tumor. Long non-coding RNA NNT-AS1 (NNT-AS1) takes crucial roles in several tumors. So, we planned to research the roles and underlying mechanism of NNT-AS1 in CCA.Results: NNT-AS1 overexpression was appeared in CCA tissues and cell lines. Proliferation was promoted by NNT-AS1 overexpression in CCLP1 and TFK1 cells. Besides, NNT-AS1 overexpression reduced E-cadherin level and raised levels of N-cadherin, vimentin, Snail and Slug. However, the opposite trend was occurred by NNT-AS1 knockdown. Further, NNT-AS1 overexpression promoted phosphatidylinositol 3 kinase (PI3K)/AKT and extracellular signal-regulated kinase (ERK)1/2 pathways. MiR-203 was sponged by NNT-AS1 and miR-203 mimic reversed the above promoting effects of NNT-AS1. Additionally, insulin-like growth factor type 1 receptor (IGF1R) and zinc finger E-box binding homeobox 1 (ZEB1) were two potential targets of miR-203.Conclusion: NNT-AS1 promoted proliferation, EMT and PI3K/AKT and ERK1/2 pathways in CCLP1 and TFK1 cells through down-regulating miR-203.Methods: CCLP1 and TFK1 cells were co-transfected with pcDNA-NNT-AS1 and miR-203 mimic. Bromodeoxyuridine (BrdU), flow cytometry, quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot were employed to detect roles and mechanism of NNT-AS1. Interaction between NNT-AS1 and miR-203 or miR-203 and target genes was examined through luciferase activity experiment.
Highlights
Cholangiocarcinoma (CCA) is an aggressive tumor coming from biliary epithelial cells, and it is divided into several anatomic subtypes: intrahepatic, hilar and extrahepatic [1]
We attempted to investigate the function of NNTAS1 in CCLP1 and TFK1 cells through transfection with pcDNA-nicotinamide nucleotide transhydrogenaseantisense RNA1 (NNT-AS1) and si-NNT-AS1
Consequents showed that levels of NNT-AS1 were apparently increased in both cells transfected with pcDNA-NNTAS1 (P < 0.01 and P < 0.001), while were notably decreased contrasted with relative control in both cells transfected with si-NNT-AS1, suggesting that the NNT-AS1 overexpression and knockdown cell models were successfully established, respectively
Summary
Cholangiocarcinoma (CCA) is an aggressive tumor coming from biliary epithelial cells, and it is divided into several anatomic subtypes: intrahepatic, hilar and extrahepatic [1]. A thorough understanding of CCA mechanism, pathogenic genes and complicated interactions of tumor microenvironments can provide optimal treatment options for patients and improve survival. Results: NNT-AS1 overexpression was appeared in CCA tissues and cell lines. Proliferation was promoted by NNT-AS1 overexpression in CCLP1 and TFK1 cells. NNT-AS1 overexpression promoted phosphatidylinositol 3 kinase (PI3K)/AKT and extracellular signal-regulated kinase (ERK)1/2 pathways. MiR-203 was sponged by NNT-AS1 and miR-203 mimic reversed the above promoting effects of NNT-AS1. Conclusion: NNT-AS1 promoted proliferation, EMT and PI3K/AKT and ERK1/2 pathways in CCLP1 and TFK1 cells through down-regulating miR-203. Methods: CCLP1 and TFK1 cells were co-transfected with pcDNA-NNT-AS1 and miR-203 mimic. Interaction between NNT-AS1 and miR-203 or miR-203 and target genes was examined through luciferase activity experiment
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