Definition of molecular determinants of prostate cancer cell bone extravasation.

Advanced prostate cancer commonly metastasizes to bone, but transit of malignant cells across the bone marrow endothelium (BMEC) remains a poorly understood step in metastasis. Prostate cancer cells roll on E-selectin(+) BMEC through E-selectin ligand-binding interactions under shear flow, and prostate cancer cells exhibit firm adhesion to BMEC via β1, β4, and αVβ3 integrins in static assays. However, whether these discrete prostate cancer cell-BMEC adhesive contacts culminate in cooperative, step-wise transendothelial migration into bone is not known.

Alpha 1,3 fucosyltransferases are master regulators of prostate cancer cell trafficking.

How cancer cells bind to vascular surfaces and extravasate into target organs is an underappreciated, yet essential step in metastasis. We postulate that the metastatic process involves discrete adhesive interactions between circulating cancer cells and microvascular endothelial cells. Sialyl Lewis X (sLe(X)) on prostate cancer (PCa) cells is thought to promote metastasis by mediating PCa cell binding to microvascular endothelial (E)-selectin.

Spatial and temporal expression of dADAR mRNA and protein isoforms during embryogenesis in Drosophila melanogaster.

Adenosine Deaminases Acting on RNA (ADARs) function to co-transcriptionally deaminate specific (or non-specific) adenosines to inosines within pre-mRNAs, using double-stranded RNAs as substrate. In both Drosophila and mammals, the best-studied ADAR functions are to catalyze specific nucleotide conversions within mRNAs encoding various ligand- or voltage-gated ion channel proteins within the adult brain. In contrast, ADARs within developing fly embryos have scarcely been studied, in part because they contain little or no editase activity, raising interesting questions as to their functional significance.