Majority of patients with metastasis die from the disease in the absence of efficient treatments. The microvascular arrest of circulating cancer cells triggers an inflammatory reaction leading to cancer cell apoptosis and cytotoxicity. However, certain cancer cells resist, and even deactivate this anti-tumor defense, and they adhere to endothelial cells through cytokine-mediated adhesion molecules. Surviving cancer cells are further supported by proliferation-stimulating factors released by tumor-activated host cells and form avascular micrometastases. Tumor-activated myofibroblasts are recruited into micrometastases to support cancer development through the specific release of proangiogenic factors and cancer cell invasion- and proliferation-stimulating factors. Moreover, tumor-activated myofibroblasts contribute to hepatic metastasis-related gene regulation. Certain metastasis-susceptible sites offer a favorable microenvironment to circulating cancer cells that supports metastasis. The capability to resist anti-tumor defense and to take advantage of host cell-derived factors are key phenotypic properties of metastasizing cancer cells. Knowledge on cancer cell regulation by microenvironment opens multiple avenues for metastasis inhibition at both subclinical and advanced stages. In addition, together with metastasis-related gene profiles revealing the existence of metastasis potential in primary tumors, new biomarkers on the prometastatic microenvironment may be helpful for the individual assessment of metastasis risk in cancer patients.
Learning objectives
- Molecular mediators of cancer metastasis.
- Steps of the cancer metastasis process
- Metastasis-related gene profiles.
- Molecular targets for anti-metastatic drug innovation
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