Table 1.
The role of MCP-1 in the metastasis of different cancers to bone.
| Type of cancer | MCP-1 involvement | Reference |
|---|---|---|
| Prostate | Docetaxel increased MCP-1 expression and this increase in expression resulted in a protective effect, decreasing the chemotherapeutic effectiveness of Docetaxel | [69] |
| MCP-1 expression by adipocytes in obese individuals associated with prostate cancer progression and invasiveness | [70] | |
| Lung | MCP-1 implicated in the promotion of CCR2+/Ly6Chi monocytes and the induction of CCR2+ endothelial cell vascular permeability in the lungs | [71] |
| Fibrocytes elicit a pre-metastatic niche-conditioning effect through the recruitment Ly6C+ monocytes via MCP-1 | [72] | |
| MCP-1 positively associated with metastasis-related bone loss | [73] | |
| Nasopharyngeal | Expression of MCP-1 higher in poorly differentiated NPC cells compared to highly differentiated NPC cells, suggesting that MCP-1 plays a role in the maturation and progression of these cancerous cells | [74] |
| Multiple myeloma | MCP-1 is over-expressed – MCP-1 expression in bone marrow stromal cells is upregulated by human myeloma cells | [75] |
| Oral squamous cell carcinoma | Associated with elevated expression of MCP-1 | [42••] |
| Inhibition of MCP-1 with its dominant-negative form, 7ND, successfully inhibited osteoclast differentiation and limited the capacity of OSCC to invade surrounding bone | [76] | |
| Myeloid leukaemia | Implicated in cell transmigration and proliferation; however, not in chemotherapy resistance | [77] |