Research Paper Advance Articles
Silencing LINC00482 inhibits tumor-associated inflammation and angiogenesis through down-regulation of MMP-15 via FOXA1 in bladder cancer
- 1 Cancer Center, The First Hospital of Jilin University, Changchun 130021, P. R. China
- 2 Department of Cardiology, The First Hospital of Jilin University, Changchun 130021, P. R. China
- 3 The First Operating Room, The First Hospital of Jilin University, Changchun 130021, P. R. China
- 4 Department of Intensive Care Unit (ICU), The First Hospital of Jilin University, Changchun 130021, P. R. China
- 5 Department of Gastrointestinal Surgery, The First Hospital of Jilin University, Changchun 130021, P. R. China
Received: March 27, 2020 Accepted: October 5, 2020 Published: December 11, 2020https://doi.org/10.18632/aging.202247
How to Cite
Copyright: © 2020 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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.