Table 2.
Proposed PODXL mechanisms in cancer metastasis.
Mechanism | Proteins That PODXL Interacts with | Cancer Type |
---|---|---|
EMT | Colocalisation and interaction with collagen I, interaction with ezrin, E-cadherin, and vimentin | Lung [63,81] |
Migration and Invasion | Colocalisation and interaction with gelsolin | Pancreatic [73] |
Binding to ezrin | Breast [13] | |
Enhancing the activation of PI3K, Ras/rac1, and MAPK signalling pathway | Pancreatic [18] | |
Activation of rac1/cdc42/cortactin signalling | Breast [82] | |
Activation of FAK | Oral squamous cell [83] | |
Increasing MMP | Breast [13] | |
Binding to selectins (E- and L-) | Colon [84]Pancreatic [66] | |
Colocalisation and interaction with CLIC5 | Liver [54] | |
Binding to dynamin-2 | Pancreatic [18] | |
Stimulating the C5aR/C5a axis | Pancreatic [85] | |
Associates with TAZ | Colon [86] | |
Extravasation from the vasculature | Binding to ezrin | Breast [87] |
Immune evasion | Inhibiting NK cell receptors Increasing the expression of MHC I molecule (HLA-ABC) |
Breast [17] |
Chemoresistance | Increasing Bmi1 | Oral tongue squamous cell [88] |