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

In this study, we aimed to identify potential lncRNA deregulations associated with breast cancer malignancy instigated by MSCs-MCF7 co-culture. We profiled expression changes of lncRNAs in MCF-7 cells during EMT induced by coculture with hAD-MSCs, and found an intergenic lncRNA with proviouly unknown function (KB-1732A1.1, we termed it LincK), which was significantly elevated. Depletion of LincK decreased the growth, migration, invasion, and EMT in breast cancer cells, while 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. LincKs can act as a sponge of mirR-200b, which inhibits its function in proliferation and metastasis. Thus we reported, for the first time, the role of LincK in control of EMT and proliferation in breast cancer. We used microarrays to detail the genes associated with LincK. Transcriptome analysis of LincK siRNA-knockdown in cultured MCF-7 cells.To detect the targeting of LincK, we used microarray to analyze changes in gene expression patterns after siRNA transfection in MCF-7 cells. 3 independent biological replicates were plated, transfected in parallel for each control and siRNA. Two different siRNAs were used.