SSeCKS/AKAP12 induces repulsion between human prostate cancer and microvessel endothelial cells through the activation of Semaphorin 3F

Biochem Biophys Res Commun. 2017 Sep 2;490(4):1394-1398. doi: 10.1016/j.bbrc.2017.07.043. Epub 2017 Jul 8.

Abstract

Metastasis remains the primary cause of prostate cancer related death. Cancer cells need to contact endothelial cells and disrupt endothelial junctions to cross the endothelium for invasion and metastasis. The suppression of heterotypic repulsion between cancer and endothelial cells allows cancer cells to invade into the surrounding tissue. Here, we demonstrate that SSeCKS/AKAP12 induced repulsion between human prostate cancer and microvessel endothelial cells, which was mediated by an angiogenesis inhibitor Semaphorin 3F. Moreover, we examined AKAP12 and Semaphorin 3F mRNA expression in 42 prostate cancer and 30 benign prostatic hyperplasia tissue samples, and found that the expression of AKAP12 and Semaphorin 3F mRNA was inversely associated with the degree of aggressiveness of prostate cancer cells and tissues. An ordinal logistic regression analysis indicates that there is a positive association between the expression of AKAP12 and Semaphorin 3F in prostate cancer, suggesting that the activation of Semaphorin 3F by SSeCKS/AKAP12 may be involved in prostate cancer progression and metastasis.

Keywords: Cell repulsion; Prostate cancer; SSeCKS/AKAP12; Semaphorin 3F.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • A Kinase Anchor Proteins / genetics
  • A Kinase Anchor Proteins / metabolism
  • Cell Cycle Proteins / genetics
  • Cell Cycle Proteins / metabolism
  • Coculture Techniques
  • Disease Progression
  • Endothelial Cells / cytology
  • Endothelial Cells / metabolism*
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Male
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism
  • Neoplasm Grading
  • Neoplasm Metastasis
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / metabolism
  • Prostate / metabolism*
  • Prostate / pathology
  • Prostatic Hyperplasia / genetics*
  • Prostatic Hyperplasia / metabolism
  • Prostatic Hyperplasia / pathology
  • Prostatic Neoplasms / genetics
  • Prostatic Neoplasms / metabolism
  • Prostatic Neoplasms / pathology
  • RNA, Messenger / genetics*
  • RNA, Messenger / metabolism
  • Signal Transduction
  • Tumor Cells, Cultured

Substances

  • A Kinase Anchor Proteins
  • AKAP12 protein, human
  • Cell Cycle Proteins
  • Membrane Proteins
  • Nerve Tissue Proteins
  • RNA, Messenger
  • SEMA3F protein, human