4.5 Article

MiR-125b promotes migration and invasion by targeting the vitamin D receptor in renal cell carcinoma

Journal

INTERNATIONAL JOURNAL OF MEDICAL SCIENCES
Volume 18, Issue 1, Pages 150-156

Publisher

IVYSPRING INT PUBL
DOI: 10.7150/ijms.49328

Keywords

Renal Cell Carcinoma; Vitamin D Receptor; MicroRNA; MiR-125b

Funding

  1. Natural Science Foundation of Fujian Province, China [2019J01590]
  2. National Natural Science Foundation of China [81372734]
  3. Special fund of Fujian Medical University for Scientific and Technological Development [FZS13035Y]
  4. Sailing Fund of Fujian Medical University [2018QH1164]
  5. The Scientific Fund of Sanming Science and Technology Bureau [N0.2018-5-1(7)]
  6. Natural Science Foundation of Fujian Province [2020J01126]

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The research findings suggest that miR-125b plays a role in promoting migration, invasion, and inhibiting apoptosis in renal cell carcinoma, and is negatively correlated with VDR.
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.

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