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LincK promotes proliferation and epithelial-to-mesenchymal transition and contributes to tumorigenesis and growth in breast cancer II

ABSTRACT: We previously reported that transwell co-culture with hAD-MSCs cells can induce an EMT progress in MCF7 cells. To identify EMT-relevant lncRNAs, we conducted transcriptome microarray analysis of MCF7 cells at Day 0, 2, 4, 6, 8 and 10 after coculture.

ORGANISM(S): Homo sapiens

PROVIDER: GSE109008 | GEO | 2019/01/09

REPOSITORIES: GEO

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Project description:BackgroundIncreasing evidence has demonstrated that mesenchymal stem cells (MSCs) play a role in the construction of tumor microenvironments. Co-culture between tumor cells and MSCs provides an easy and useful platform for mimicking tumor microenvironments and identifying the important members involved in tumor progress. The long non-coding RNAs (lncRNAs) have been shown to regulate different tumorigenic processes. In this study, we aimed to examine functional lncRNA deregulations associated with breast cancer malignancy instigated by MSC-MCF-7 co-culture.MethodsThe microarrays were used to profile the expression changes of lncRNAs in MCF-7 cells during epithelial-mesenchymal transition (EMT) induced by co-culture with MSCs. We found that an intergenic lncRNA KB-1732A1.1 (termed LincK, partly overlapped with GASL1) was significantly elevated. To investigate the biological function of LincK, the expression of EMT markers, cell migration, invasion, proliferation, and colony formation were evaluated in vitro and xenograft assay in nude mice were performed in vivo. Furthermore, we detected LincK expression in clinical samples using RNAscope® technology and verified aberrant expression of LincK in breast cancer data sets from The Cancer Genome Atlas (TCGA) by bioinformatic analysis. The underlying mechanisms of LincK were investigated using mRNA microarray analyses, Western blot, RNA pull down, and RNA immunoprecipitation.ResultsLincK induced an EMT progress in breast cancer cells (BCC) MCF-7, MDA-MB-453, and MDA-MB-231. The depletion of LincK decreased the growth, migration, and invasion in BCC, whereas the overexpression of LincK exerted the opposite effects. Moreover, knockdown of LincK repressed tumorigenesis, and ectopic expression of LincK promoted tumor growth in MCF-7 xenograft model. LincK ablation in MDA-MB-231 cells dramatically impaired lung metastasis when incubated intravenously into nude mice. Further, LincK was frequently elevated in breast cancer compared with normal breast tissue in clinical samples. Mechanistically, LincK may share common miRNA response elements with PBK and ZEB1 and regulate the effects of miR-200 s.ConclusionLincK plays a significant role in regulating EMT and tumor growth and could be a potential therapeutic target in breast cancer.

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LincK promotes proliferation and epithelial-to-mesenchymal transition and contributes to tumorigenesis and growth in breast cancer II

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