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Fig. 1 | Journal of Translational Medicine

Fig. 1

From: Tumor microenvironment differences between primary tumor and brain metastases

Fig. 1

Schematic representation of protein expression, molecular pahtways, facilitators and mutations involved in the genesis of brain metastases from melanoma, breast and lung cancer. Breast cancer cells: Upregulated expression of A.R. (androgen receptor), P.R. (progesterone receptor) and E.R .(estrogen receptor) in the primary tumor. miRNA-509 → Rhoc/TNF pathway → BBB permeability/MMP9 in Circulating tumor cells (CTCs). miRNA-31, -126,-335 suppress metastasic spread. miRNA-7 downregulates KLFM pathway in stem cells. Cathepsin S (CTSS) proteolytic processing of the junction adhesion molecule (JAM). The N-acetylgalactosaminidase α2,6 sialyltransferase 5 (ST6GALNAC5) has been identified as a facilitator of tumor cell/brain endothelial adhesion. The chemokine receptor CXCR4 and its ligand CXCL12 increase vascular permeability and activation of the PI-3K/AKT pathway. Lung Cancer cells: Upregulated EGFR, PI3K, Keap-1, Nfr2, P300, Tp53, Rad54L2, NTRK3, and TARX. miRNA-328 upregulates the PKACA pathway. miRNA-378 is upregulated and miRNA-145 downregulated. IncRNA MALAT1 induces EMT and HOTAIR high expression in BM. The Rho kinase signaling, involved in intracellular junction disruption, has been found activated in this transendothelial migration. Melanoma Cancer cells: Upregulated BRAF mutation, induce PI3K/AKT pathway. miRNA-210 was overexpressed in exosomes of BM cells and miRNA 19a and miRNA-29c were downregulated in exosomes BM cells. In CTC, the membrane-bound melanotransferrin correlates with brain endothelial adhesion

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