SSeCKS/AKAP12 Induces Repulsion Between Human Prostate Cancer and Microvessel Endothelial Cells Through the Activation of Semaphorin 3F
Publisher: Biochemical and Biophysical Research Communications, vol. 490, issue 4
- Metastasis remains the primary cause of prostate cancer (CaP) related death.
- SSeCKS/AKAP12 induced repulsion between prostate cancer and microvessel endothelial cells through Semaphorin 3F.
- The activation of Semaphorin 3F by SSeCKS/AKAP12 may be involved in CaP metastasis.
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.