| Metastatic site | Phenotype | Signalling | Ref. |
---|---|---|---|---|
Breast cancer | Lymph nodes | Significant change of P-cad expression in the lymph nodes vs. primary tumour | Â | Adamczyk et al., 2012 [69] |
 |  | Invasion, migration motility | Soluble P-cad, MMPs | Ribeiro et al., 2010 [75] |
 |  | Stem cell activity Adhesion to laminin | α6β 4-integrin, FAK, Src, Akt | |
 |  | Increased glycolysis and acid resistance | CA-IX, Glut-1 | Sousa et al., 2014 [94] |
Ovary | Peritoneum | P-cad necessary for adhesion of CaOV-3 cells to the peritoneum | P-cad/β 1-integrin | Ip et al., 2014 [85] |
 | Peritoneum | P-cad necessary for adhesion of CaOV-3 and OVCAR-3 (to ECM and peritoneal cells) P-cad inhibition attenuated tumour growth, ascites formation, and the number of metastatic implants | Gonadotropin-releasing hormone induces P-cadherin expression and α2, α5 and β1 integrin | Cheung et al., 2013 [70] |
 | Peritoneum | P-cad necessary for the activation of the IGF-1R by GnRH in CaOV-3 cells P-cad and p-IGF-1R coexpression was significantly stronger in metastasis compared with primary tumours | p120 phosphorylation by Gonadotropin-releasing hormone is dependent on P-cadherin and IGF-1R interaction | Cheung et al., 2011 [86] |
Colon | Liver | Increased in liver metastasis of colon cancer, compared with the primary cancer tissue; Knock-down of P-cadherin in colon cancer cells (LOVO) resulted in developing fewer liver metastatic foci | P-cad inhibition in colon cancer cells (LOVO) induced the up-regulation of E-cadherin and the down-regulation of β-catenin and its downstream target molecules, including survivin and c-Myc. | Sun et al., 2011 [71] |
Prostate cancer | Bone | P-cad expression in primary tumour associated with shorter time to skeletal metastasis | Â | Gravdal et al., 2007 [72] |
Gallbladder adenocarcinoma | Lymph nodes | P-cad expression in primary adenocarcinoma and squamous cell/adenosquamous carcinoma associated with lymph node metastasis | Â | Yi et al. 2014 [68] |