Haohong Shi1, Changting Yan2, Yuanyuan Chen3, Zhuoqun Wang4, Junhong Guo5, Hao Pei1. 1. Department of Anesthesiology, Children's Hospital of Fudan University, National Children's Medical Center Shanghai City, China. 2. Department of Anesthesiology, Liaocheng Dongchangfu District Maternity and Child Health Care Hospital Liaocheng, Shandong Province, China. 3. Department of Anesthesiology, Yancheng Maternity and Child Health Care Hospital Yancheng, Jiangsu Province, China. 4. Department of Anesthesiology, Huashan Hospital, Fudan University Shanghai City, China. 5. Department of Nursing, Dongchangfu People's Hospital Liaocheng, Shandong Province, China.
Abstract
OBJECTIVE: Renal cell carcinoma (RCC) is one of the most common and life-threatening cancers in the world. Accumulating evidence suggest propofol inhibits the initiation and development of cancers. The main focus of the study was to explore the effect of propofol on RCC and its mechanism of action. METHODS: In this study, different doses of propofol were used to treat human RCC cell lines i.e., OSRC-2 and SW839. Western blot and trans-well assays were used for the evaluation of RCC cell invasion, proliferation, migration, and transition of epithelial to mesenchymal (EMT). RCC cells following 5 μmol/L propofol treatment for 24 h were applied in the subsequent experiments. Expression of MicroRNAs-363 (miR-363) in cells with or without propofol treatment were analyzed. The expression of Snail1, Vimentin, N-cadherin, and E-cadherin in RCC cells was measured, and then the effect of loss-of-function of miR-363 and gain-of-function of Snail on RCC cells were analyzed. The targeted relationship between miR-363 and Snail1 was investigated using luciferase assay and RIP, RNA pull down. RESULTS: Propofol reduced the migration, proliferation, invasion and EMT of RCC cells in a dose-dependent way. Propofol elevated miR-363 expression but reduced Snail1 expression, and it reduced Vimentin and N-cadherin but increased E-cadherin expression in RCC cells. miR-363 directly bounds to Snail1. miR-363 inhibition or Snail1 promotion reversed propofol-inhibited malignant behaviors of RCC cells. CONCLUSION: Our study found that propofol could inhibit invasion, migration, proliferation and EMT of RCC cells by promoting miR-363 expression and suppressing Snail1 expression. AJTR
OBJECTIVE:Renal cell carcinoma (RCC) is one of the most common and life-threatening cancers in the world. Accumulating evidence suggest propofol inhibits the initiation and development of cancers. The main focus of the study was to explore the effect of propofol on RCC and its mechanism of action. METHODS: In this study, different doses of propofol were used to treat humanRCC cell lines i.e., OSRC-2 and SW839. Western blot and trans-well assays were used for the evaluation of RCC cell invasion, proliferation, migration, and transition of epithelial to mesenchymal (EMT). RCC cells following 5 μmol/L propofol treatment for 24 h were applied in the subsequent experiments. Expression of MicroRNAs-363 (miR-363) in cells with or without propofol treatment were analyzed. The expression of Snail1, Vimentin, N-cadherin, and E-cadherin in RCC cells was measured, and then the effect of loss-of-function of miR-363 and gain-of-function of Snail on RCC cells were analyzed. The targeted relationship between miR-363 and Snail1 was investigated using luciferase assay and RIP, RNA pull down. RESULTS:Propofol reduced the migration, proliferation, invasion and EMT of RCC cells in a dose-dependent way. Propofol elevated miR-363 expression but reduced Snail1 expression, and it reduced Vimentin and N-cadherin but increased E-cadherin expression in RCC cells. miR-363 directly bounds to Snail1. miR-363 inhibition or Snail1 promotion reversed propofol-inhibited malignant behaviors of RCC cells. CONCLUSION: Our study found that propofol could inhibit invasion, migration, proliferation and EMT of RCC cells by promoting miR-363 expression and suppressing Snail1 expression. AJTR