Rap2B promotes cell proliferation, migration and invasion in prostate cancer

Med Oncol. 2016 Jun;33(6):58. doi: 10.1007/s12032-016-0771-7. Epub 2016 May 6.

Abstract

Rap2B, a member of the Ras family of small GTP-binding proteins, reportedly presents a high level of expression in various human tumors and plays a significant role in the development of tumor. However, the function of Rap2B in prostate cancer (PCa) remains unclear. We elucidated the stimulative role of Rap2B in PCa cell proliferation, migration and invasion by means of the CCK-8 cell proliferation assay, cell cycle analysis and transwell migration assay. Western blot analysis uncovered that elevated Rap2B leads to increased phosphorylation levels of FAK, suggesting that FAK-dependent pathway might be responsible for the effect of Rap2B on PCa cells migration and invasion. Inversely, FAK-specific inhibitor (PF-573228) can abort Rap2B-induced FAK phosphorylation. In vivo experiment confirmed that Rap2B positively regulated PCa growth and metastasis, as well as the expression of phosphorylated FAK. Collectively, these findings shed light on Rap2B as a potential therapeutic target for PCa.

Keywords: FAK; Migration; Prostate cancer; Rap2B.

MeSH terms

  • Animals
  • Cell Line, Tumor
  • Cell Movement / physiology
  • Cell Proliferation / physiology
  • Focal Adhesion Kinase 1 / metabolism
  • Heterografts
  • Humans
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • Neoplasm Invasiveness
  • Neoplasm Metastasis
  • Phosphorylation
  • Prostatic Neoplasms / enzymology*
  • Prostatic Neoplasms / pathology*
  • rap GTP-Binding Proteins / metabolism*

Substances

  • Focal Adhesion Kinase 1
  • PTK2 protein, human
  • RAP2B protein, human
  • rap GTP-Binding Proteins