Xinbo Du1, Jianguo Shi2. 1. Department of Urology, the First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning, 121001, People's Republic of China. 2. Department of Urology, the First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning, 121001, People's Republic of China. jzykdxsjg@163.com.
Abstract
BACKGROUND: Renal cell carcinoma or RCC is a type of malignancy commonly occurred in the human kidney especially in the adults. The pathogenesis of RCC involves the complex networking of multiple signaling pathways, and the underlying molecular mechanisms remain largely unclear. OBJECTIVES: This study aimed to elucidate the regulatory functions of UBA2 and explore its potential downstream molecules during the tumor progression in RCC. METHODS: In this paper, the expression of UBA2 and associated molecules was examined by RT-qPCR and western blotting. The proliferative activity of RCC cells was determined using CCK-8 assay and immunofluorescence staining of proliferation-related marker Ki-67. Moreover, the cell distribution and apoptosis were evaluated by flow cytometry. RESULTS: Our results revealed the upregulation of UBA2 in RCC tissues and cells, and the high-expression of UBA2 was also associated with bigger tumor size, more advanced stage, and poorer overall survival in RCC patients. In addition, UBA2 knockdown was able to suppress the growth of RCC cells and induced cell cycle arrest at G0/G1 phase. Furthermore, the p53 signaling could be the novel target of UBA2 in RCC, and UBA2 affected the biological behaviors of RCC cells in a p53-dependent manner. CONCLUSION: In summary, UBA2 was able to enhance the proliferation, inhibit the apoptosis, and suppress cell cycle arrest in RCC cells by targeting the p53 pathway.
BACKGROUND: Renal cell carcinoma or RCC is a type of malignancy commonly occurred in the human kidney especially in the adults. The pathogenesis of RCC involves the complex networking of multiple signaling pathways, and the underlying molecular mechanisms remain largely unclear. OBJECTIVES: This study aimed to elucidate the regulatory functions of UBA2 and explore its potential downstream molecules during the tumor progression in RCC. METHODS: In this paper, the expression of UBA2 and associated molecules was examined by RT-qPCR and western blotting. The proliferative activity of RCC cells was determined using CCK-8 assay and immunofluorescence staining of proliferation-related marker Ki-67. Moreover, the cell distribution and apoptosis were evaluated by flow cytometry. RESULTS: Our results revealed the upregulation of UBA2 in RCC tissues and cells, and the high-expression of UBA2 was also associated with bigger tumor size, more advanced stage, and poorer overall survival in RCC patients. In addition, UBA2 knockdown was able to suppress the growth of RCC cells and induced cell cycle arrest at G0/G1 phase. Furthermore, the p53 signaling could be the novel target of UBA2 in RCC, and UBA2 affected the biological behaviors of RCC cells in a p53-dependent manner. CONCLUSION: In summary, UBA2 was able to enhance the proliferation, inhibit the apoptosis, and suppress cell cycle arrest in RCC cells by targeting the p53 pathway.