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Molecular Regulation Of Bone Marrow Metastasis In Prostate And Breast Cancer

2762 words - 12 pages

It has been shown that platelets, which are transient cells in BM microenvironment, are important for metastasis of a variety of solid tumors (Figure 1). Platelets bind circulating tumor cells, protecting them against anoikis (a type of programmed cell death occurring due to detachment of the cell from surrounding ECM) as well as against the innate immune system (2, 56, 57). Platelet-derived TGF-β and direct contact between platelets and tumor cells synergistically activate TGF-β/Smad and NF-κB pathways, leading to epithelial-mesenchymal transition (EMT), increased invasion and metastasis (58). In addition, during platelet aggregation by breast cancer cells, platelet-derived lysophosphatidic ...view middle of the document...

Patients with metastatic PCa have significantly lower expression of miR-143 and miR-145 compared with patients without metastasis. Upregulation of miR-143 and miR-145 decreases the invasion capacity of PC-3 cells in vitro and in vivo. EMT is suppressed through inhibition of mesenchymal markers vimentin and fibronectin and is increased in E-cadherin (65). Increased expression of miRNA -143 and -145 inhibits cell viability and colony formation in bone metastasis of PC-3 cells isolated from PCa. Moreover, these miRNAs suppress tumor cell formation, expression of cancer stem cells (CSC) markers and stemness factors such as CD133, CD44, Oct4, C-Myc and K1f4 in PC-3 cells, ultimately preventing bone invasion and tumorigenicity (66). Stemness is described as a pattern of gene expression that is common among all stem cells and distinguishes them from ordinary cells (67). Human enhancer of filamentation 1 (HEF1) gene is a target of miR-145, and its expression is negatively correlated with miR-145 in primary PCa and bone metastasis. HEF1 expression is associated with an elevated level of PSA (68). MiR-203 expression in bone metastatic PCa is significantly attenuated compared to normal tissue, and its re-expression suppresses metastasis in PCa in vitro. Indeed, miR-203 is an anti-metastatic miRNA. Ectopic expression of miR-203 leads to expression repression of Runx2 and Smad4 (69). Runx2 and Smad4 are critical in regulating the expression of genes involved in bone formation, and are ectopically expressed in bone metastases and tumors (70). The serum level of miR-141 is increased in patients with bone metastatic PCa, and is related to bone metastatic lesion. A correlation has been reported between increased serum levels of miR-141 and the level of ALP but not that of PSA (71). As a result, the serum miRNA level can function as a new biomarker for diagnosis and assessment of metastasis. Expression of miRNAs -508-5p, -145, -143, 33a and -100 in bone metastasis is severely decreased compared with primary tumors of prostate (72). MiR-218 increases the Wnt activity and abnormal expression of OB genes by downregulating three inhibitors of this pathway including Sclerostin (SOST), DKK2 and secreted frizzled related-protein 2 (SFRP2) during osteogenesis, which participate in the homing and growth of metastasized cells to the bone (73). MiR-218 expression is stimulated in response to Wnt signaling, and is upregulated in metastatic breast cancer cells but not in normal epithelial mammary cells (73). Raf kinase inhibitor protein (RKIP) belongs to evolutionarily conserved phosphatidylethanolamine binding protein (PEBP) family and negatively modulates the MAP kinase (MAPK), G protein-coupled receptor kinase-2 and NF-κB signaling cascades (74). RKIP has been found as a suppressor of PCa metastasis in a mouse model, and decreased expression of it is associated with increased invasion capacity of prostate cancer cells through activation of MEK and ERK (75). RKIP expression...

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