A malignant tumor predominantly consists of proliferating cells, a smaller percentage of the cells in the resting phase G0 and G1, as well as necrotic and/or apoptotic cells. It is a heterogeneous structure with the ability to metastasize which includes the acquisition of additional genetic mutation, migration ability or the production of MMP (metalloproteinase). Unfortunately, at present it is impossible to find tissue cells with clearly specify features of metastasis in the tumor, and therefore it requires more intense research in this direction. This paper describes the stages of the cancer cell migration from a place of origin, the effect of which is to create metastatic deposits. The metastatic process is compared to the adoption of “seedlings in the soil” (seed and soil). Complementary adhesion molecules are expressed in both the metastatic cells as well as in the target organ cells. The stroma of an organ decides whether cancer cells are adopted. It should be characterized by the absence of proteinase inhibitors, the presence of various growth factors and the ability of neoangiogenesis. Each metastasis can be a point of departure for further metastasis. It has been also describes a number of metastatic mechanisms, i.e. involved in the process of chemokines, adhesion molecules, neoangiogenesis, types of Lewis antigens a, b, x, y, cancer stem cells (CSC), and presents the phenomenon of transmigration through the blood vessels, which is similar to the migration of granulocytes in the system. Tumor cell clones with a high metastatic potential differ from low metastatic counterparts with regard to pheno- and genotypic features. This means that not all of the malignant tumors have the same invasiveness or metastatic potential. Therefore, special attention was paid to the role of genes in metastatic neoplasia (genes: SDF1, BRMS1, MET, IAP-4, KAI-1, KISS-1, NM-23-H1, UGT8, alpha Klotho). The newly discovered intercellular connections are also mentioned, i.e. membrane nanotubes (tunnel – TNTs), enabling the mitochondrial transport between cells, mtDNA transfer and its mutation, as well as mediate in the phenomenon of MDR (multidrug resistance), i.e. removal the xenobiotics from the cells (such as cytostatics), which explains the failure of cancer chemotherapy. Unfortunately recognition of all metastatic molecular mechanisms has not been fully explained to date.
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