Transcript-level regulation of MALAT1-mediated cell cycle and apoptosis genes using dual MEK/Aurora kinase inhibitor "BI-847325" on anaplastic thyroid carcinoma.

摘要: Anaplastic thyroid carcinoma (ATC) is the most lethal malignancy in carcinomas. Long non-coding RNAs (lncRNAs) are a member of RNAs, regulating expression gene. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) an onco-lncRNA that overexpressed several carcinomas including ATC. Evidence showed MALAT1 has crucial function apoptosis, and cell cycle progression. In order to take advantage 3D culture system cancer investigation, we have used vitro ATC model determine effect dual MEK/Aurora kinase inhibitor BI-847325 anticancer drug on fundamental molecular mechanisms MALAT1-mediated gene regulation this study, lines (C643 SW1736) were grown alginate scaffold. Encapsulated cells treated by BI-847325. Changes MALAT1, Mcl1, miR-363-3p, cyclinD1 measured qRT-PCR. following treatment was significantly downregulated C643 SW1736 lines. Reversely, miR-363-3p upregulated both Mcl1 after Moreover, not reduced line. Additionally, cyclin D1 Altogether, result study first report MALAT1’s suggested which inhibits MEK Aurora family could be effective against genes involved apoptosis MALAT1and its downstream genes.