MiR-193b inhibits the growth and metastasis of renal cell carcinoma by targeting IGF1R

Artif Cells Nanomed Biotechnol. 2019 Dec;47(1):2058-2064. doi: 10.1080/21691401.2019.1620251.

Abstract

Objective: To explore the effects of miR-193b on cell proliferation, migration, invasion and tumourigenicity of renal cell carcinoma, and the underlying molecular mechanisms. Methods: The expression of miR-193b and IGF1R was detected by quantitative real-time polymerase chain reaction (qRT-PCR). MTT assay was used to detect cell viability. The migration and invasion abilities were measured by transwell assay. Western blot was used to detect the protein expression of IGF1R. Murine xenograft model was established using Caki-1cells transfected with miR193b. Results: The expression of miR-193b was significantly down-regulated in renal cell carcinoma tissues and cells while the expression of IGF1R was obvious increased in tissues. Overexpression miR-193b or knockdown of IGF1R significantly inhibited the abilities of cells proliferation, migration and invasion in renal cell carcinoma. MiR-193b directly targeted IGF1R and inhibited its expression in vitro and vivo. Up-regulation miR-193b inhibits cells proliferation, migration and invasion of renal cell carcinoma by targeting IGF1R. In addition, overexpression miR-193b significantly inhibited tumour growth in nude mice. Conclusion: miR-193b can inhibit the growth and metastasis of renal cell carcinoma by targeting decreasing IGF1R expression, which provides a new target for the prevention and treatment of renal cell carcinoma.

Keywords: IGF1R; invasion; kidney cancer; miR-193b; migration.

MeSH terms

  • Animals
  • Base Sequence
  • Carcinogenesis / genetics
  • Carcinoma, Renal Cell / genetics
  • Carcinoma, Renal Cell / pathology*
  • Cell Line, Tumor
  • Cell Movement / genetics
  • Cell Proliferation / genetics
  • Cell Transformation, Neoplastic
  • Humans
  • Kidney Neoplasms / genetics
  • Kidney Neoplasms / pathology*
  • Mice
  • MicroRNAs / genetics*
  • Neoplasm Metastasis / genetics
  • Receptor, IGF Type 1
  • Receptors, Somatomedin / genetics*

Substances

  • IGF1R protein, human
  • MIRN193 microRNA, human
  • MicroRNAs
  • Receptors, Somatomedin
  • Receptor, IGF Type 1