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Background  Bladder cancer (BC) is a common type of cancer that involves tumors of the urinary system and poses a serious threat to human health. Long noncoding RNAs (lncRNAs) have emerged as crucial biomarkers and regulators in many cancers. Novel lncRNA biomarkers in BC urgently need to be investigated in regard to its function and regulatory mechanisms.    Methods  Identification of differentially expressed lncRNAs in BC tissue was performed via microarray analysis. To investigate the biological functions of LINC00612, loss-of-function and gain-of-function experiments were performed in vitro and in vivo. Bioinformatics analysis, dual-luciferase reporter assays, AGO2-RIP assays, RNA pull-down assays, real-time quantitative PCR (RT-qPCR) arrays, fluorescence in situ hybridization assays, and western blot assays were conducted to explore the underlying mechanisms of competitive endogenous RNAs (ceRNAs).    Results   LINC00612  was upregulated in BC tissues and cell lines. Functionally, downregulation of  LINC00612  inhibited cell proliferation and invasion in vitro and in vivo, whereas overexpression of  LINC00612  resulted in the opposite effects. Bioinformatics analysis and luciferase assays revealed that  miR-590  was a direct target of  LINC0061 , which was validated by dual-luciferase reporter assays, AGO2-RIP assays, RNA pull-down assays, RT-qPCR arrays, and rescue experiments. Additionally,  miR-590  was shown to directly target the PHD finger protein 14 ( PHF14 ) gene.  LNIC00612  modulated the expression of E-cadherin and vimentin by competitively sponging  miR-590  to elevate the expression of  PHF14 , thus affecting BC cellular epithelial-mesenchymal transition (EMT).    Conclusions  Our results indicate that  LINC00612  enhances the proliferation and invasion ability of BC cells by sponging  miR-590  to upregulate  PHF14  expression and promote BC cellular EMT, suggesting that  LINC00612  may act as a potential biomarker and therapeutic target for BC.

LINC00612 enhances the proliferation and invasion ability of bladder cancer cells as ceRNA by sponging miR-590 to elevate expression of PHF14