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.