**3. Concluding remarks**

As metastatic mechanisms are better understood at a molecular level, it will be significantly easier for physicians to use these mechanisms as a treatment goal [90]. The identification of tissue‐specific signals involved in metastatic progression will open the way to new therapeutic strategies. For this purpose, the authors [91] reviewed recent progress in the field, with particular emphasis on the mechanisms of organ‐specific dissemination and colonization of breast cancer (**Figure 5**). Despite what has been described so far, it may not be possible to estimate exactly which cancer type may metastasize. But a noteworthy area of forthcoming cancer research will be to determine whether abnormal ECM could be an effective cancer therapeutic target. So we should understand how ECM composition and organization are normally maintained and how they may be deregulated in cancer. Then, we may protect the ECM as a castle against to invasion of cancer.

**Figure 5.** Gene mediating organ‐specific breast cancer metastasis. Breast cancer genes promoting organ‐specific meta‐ stasis to bone, lung, and brain have been identified. They include proinflammatory molecules and chemokines/recep‐ tors (e.g., COX‐, CXCL12/CXCR4), matrix‐degrading and modifying enzymes (e.g., MMP1/2, LOX), adhesion and extracellular matrix molecules (e.g., VCAM‐1, TNC, OPN), transcription factors (e.g., ID1, KLF17), intracellular signal‐ ing proteins (e.g., SRC, NF‐\_B), and cell communication proteins (JAGGED1, CTGF). Some genes promote seeding (e.g., ST6GALNAC5, AGPTL4), whereas others promote colonization (e.g., OPN, CXCR4) (see ref. [91]).
