3.2
Impact Factor
Int J Med Sci 2021; 18(1):150-156. doi:10.7150/ijms.49328 This issue Cite
Research Paper
1. Department of Urology, Affiliated Sanming First Hospital of Fujian Medicine University, Sanming, Fujian 365100, China.
2. Department of Medical and Radiation Oncology, Affiliated Sanming First Hospital of Fujian Medicine University, Sanming, Fujian 365100, China.
Purpose: To investigate the expression of miR-125b and vitamin D receptor (VDR) in renal cell carcinoma (RCC) and assess the biological function of miR-125b in RCC.
Methods: We used quantitative real-time polymerase chain reaction (RT-PCR) to detect the expression of nucleic acids and western blotting to analyze the protein abundance in RCC cell lines. MiR-125b mimic and inhibitor were employed to investigate the function and behavior of miR-125b in RCC cell lines. The relationship between miR-125 and VDR was verified using luciferase assays.
Results: Overexpression of miR-125b promoted migration and invasion and prevent cell apoptosis in ACHN cells. In contrast, miR-125b deficiency suppressed migration and invasion and induced cell apoptosis in 786-O cells. Luciferase assays indicated the interaction between miR-125b and VDR. In collected samples, miR-125b was significantly higher in RCC tissues and negatively correlated to VDR (r=-0.444, p=0.04).
Conclusion: MiR-125b displays an oncogene profile in RCC, patients with high expression of miR-125b should be a more frequent follow-up. MiR-125B may be a potential therapeutic target for RCC.
Keywords: Renal Cell Carcinoma, Vitamin D Receptor, MicroRNA, MiR-125b