Abstract
The adenosine A2b receptor (A2bR) was considered to play an oncogenic role in many human malignancies. However, the expression and molecular function of A2bR in bladder urothelial carcinoma (BUC) have not been well elucidated. Herein, we found that the expression of A2bR was higher than other adenosine receptors in BUC tissues and cells, and it was upregulated in BUC tissues compared with matched normal bladder tissues. Furthermore, high expression of A2bR was associated with poor prognosis of patients with BUC. In addition, suppression of A2bR inhibited the proliferation, migration and invasion of BUC cells and arrested the cell cycle at the G1 phase. Finally, we demonstrated that downregulation of A2bR inhibited the proliferation, migration and invasion of BUC in part via the MAPK signaling pathway, increasing the levels of P21 but decreasing the levels of cyclin B1, D, E1, MMP-2 and MMP-9. Overexpression of MMP-2 could rescue BUC cells migration and invasion. Thus, the present study indicates that A2bR may play a potential oncogenic role in BUC progression and act as a potential biomarker to identify BUC patients with poor clinical outcomes.
Highlights
Bladder urothelial carcinoma (BUC) is the second most common genitourinary malignancy leading causes of cancer-related death in western countries [1]
Western blotting assay showed that A2b receptor (A2bR) was highly expressed in these fresh BUC tissues compared to the matched normal urothelial bladder epithelial tissues (Figure 1C)
It has been documented that the expression level of A2bR was the highest among the four adenosine receptor subtypes in different ovarian and prostate cancer cell lines [9, 13]
Summary
Bladder urothelial carcinoma (BUC) is the second most common genitourinary malignancy leading causes of cancer-related death in western countries [1]. Surgical treatment is the main method for patients with non-muscle invasive bladder cancer (NMIBC) or muscleinvasive bladder cancer (MIBC). Despite advances in surgical technique, the long-term prognosis of BUC patients after treatment is still poor. It has been reported about 1/3 of NMIBC patients would relapse and progress, and the 5-year cancer-specific survival is just only 50-60% for MIBC [2,3,4]. The therapeutic response for patients with advanced BUC to radiotherapy or chemotherapy remains unsatisfactory. It is important to understand the underlying molecular mechanisms and identify new promising biomarkers that can be used to define the progressive and metastatic potential
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