From: Factors involved in cancer metastasis: a better understanding to “seed and soil” hypothesis
POSTN expressed in stroma recruits Wnt ligands and thereby increases Wnt signaling in cancer stem cells.
MMP9 is specifically induced in pre-metastatic lung endothelial cells and macrophages, thus promoting metastasis.
Macrophage binding to receptor VCAM-1 in cancer cells transmits survival signals.
CCL5 expression enhances lung colonization by recruiting innate immune cells to the metastatic microenvironment.
Upregulation of chemoattractants and recruitment of myeloid cells facilitate the pre-metastatic niche formation.
Remodel the pre-metastatic lung into an inflammatory and proliferative environment, thus diminishes immune protection.
Myeloid Progenitor Cells
Versican induces mesenchymal to epithelial transition of metastatic cancer cells by attenuating phospho-Smad2 levels.
Neutrophil-derived leukotrienes aid lung colonization by selectively expanding cancer cells with tumorigenic potential.
PHD proteins function in T cells promoting lung colonization by establishing an immunologically tolerant metastatic niche.
Hepatic stellate cells (HSCs)
HSCs play a critical role in mediating pro-metastatic niche.
Metastasis-associated macrophages (MAMs)
MAMs activate resident hepatic stellate cells (hStCs) to transition into myofibroblasts, thus promoting metastasis.
Hepatic sinusoidal endothelial cells (HHSECs)
MIF enhances migration and EMT and facilitates proliferation and apoptotic resistance in cancer cells.
Angiopoietin-like 6 accumulates in normal vessels and interacts with the cancer cell, thus promoting colonization.
LSECtin expressed in liver promotes colon carcinoma cell adhesion and migration.
BMDCs upregulate fibronectin in resident fibroblasts, facilitating the pre-metastatic niche formation.
Osteogenic niche activates the mTOR pathway in cancer cells, promoting bone colonization.
Upregulation of CCL5 and MMP in osteocytes promotes cancer invasion and growth.
Extracellular ATP adenosine
ATP and adenosine released by osteocytes promotes cancer cell migration, growth and metastasis.
Extracellular matrix secreted by astrocyte stimulates cancer cell proliferation and EMT process.
Astrocyte-derived molecules facilitate metastasis by enhancing invasion of cancer cell.
Astrocyte-derived factors induce PTEN loss in cancer cells, promoting brain metastasis outgrowth.