Abstract
Bladder cancer is a common urothelial cancer. Through proteomic approaches, calreticulin (CRT) has been identified as a urinary marker for bladder cancer. Calreticulin is a multifunctional Ca2+‐binding molecular chaperone in endoplasmic reticulum (ER) and regulates various cellular functions such as Ca2+ homeostasis, gene expression, and cell adhesion. In the present study, J82 bladder cancer cells stably transfected with RNAi of CRT were generated (J82 CRT‐RNAi) to investigate the physiological effects of CRT in bladder tumor. The results showed that knockdown of CRT expression suppressed cell proliferation, migration and adhesion. We further demonstrated that the mRNA expression and protein secretion levels of vascular endothelial growth factor‐A (VEGF‐A), an important angiogenic factor, were also decreased in these cells. In addition, we also observed that compared to control vector transfected cells, tumors derived from J82 CRT‐RNAi cells were significantly smaller in nude mice. These results suggested that CRT may play an important role in bladder tumor formation.
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