Silencing LINC00482 inhibits tumor-associated inflammation and angiogenesis through down-regulation of MMP-15 via FOXA1 in bladder cancer.

Multiple studies have previously demonstrated that long intergenic non-coding RNAs (lincRNAs) play an important role in the development of bladder cancer. However, little is known regarding the underlying molecular mechanisms of LINC00482 functions in bladder cancer. The current study aimed to elucidate the role of LINC00482 in the progression of bladder cancer. The initial step was to detect the expressions of LINC00482 and MMP15 in bladder cancer cells and tissue. According to the results from the RT-qPCR, LINC00482 and MMP15 were both highly expressed in bladder cancer cells and tissue. The relationship among LINC00482, FOXA1 and MMP15 was studied via dual-luciferase reporter assay. LINC00482 was positively correlated with MMP15. LINC00482 promoted MMP15 expression by recruiting FOXA1. Using the gain- and loss-of-function approaches, silencing of LINC00482 resulted in the downregulation of VEGF and NF-κB protein levels, decreased expression of inflammatory factors, and inhibited angiogenesis. Silencing of LINC00482 also suppressed tumor-associated inflammation and angiogenesis in vivo, which was found to be reversed by the overexpression of MMP15. The present study demonstrated that LINC00482 induced the expression of MMP15 by interacting with FOXA1, thereby contributing to the inflammation and angiogenesis in bladder cancer.