Metastasis Suppressors and the Tumor Microenvironment

The most dangerous attribute of cancer cells is their ability to metastasize. Throughout the process of metastasis, tumor cells interact with other tumor cells, host cells and extracellular molecules. This brief review explores how a new class of molecules – metastasis suppressors – regulate tumor cell–microenvironmental interactions. Data are presented which demonstrate that metastasis suppressors act at multiple steps of the metastatic cascade. A brief discussion for how metastasis suppressor regulation of cellular interactions might be exploited is presented

The effect of traverse speed on deposition efficiency of cold sprayed Stellite 21

Cold spraying of Stellite 21 powder on low carbon steel is performed to investigate the effect of traverse speed on the deposition efficiency (DE) of high-temperature alloys. Based on the simulation of particles' impact temperature and velocity, the initial experiments are performed at different gas pressures (32 and 40bar), temperatures (800 and 730°C), and stand-off distances (10, 25, and 40mm) at a constant traverse speed of 20mm.s-1. The experiments showed that high pressure, temperature, and short stand-off distance are preferred. The wipe test results indicated a potential of high DE at lower deposition flux over the substrate surface area at the first layer deposition. Thus, new tests are carried out at different traverse speeds ranging from 20 to 400mm.s-1 to adjust the deposition flux over the surface area of the substrate. The effect of traverse speed on DE and coating characteristics such as porosity and microhardness is studied as well. The results showed that the lower DE at lower traverse speed is related to the erosion of bonded particles due to the subsequent particles' impact. By increasing the traverse speed from 20 to 300mm.s-1, the DE increased more than twice. Induction time extension at higher traverse speed led to lower DE at 400mm.s-

Cyclin-dependent kinase-mediated phosphorylation of breast cancer metastasis suppressor 1 (BRMS1) affects cell migration

Expression of Breast Cancer Metastasis Suppressor 1 (BRMS1) reduces the incidence of metastasis in many human cancers, without affecting tumorigenesis. BRMS1 carries out this function through several mechanisms, including regulation of gene expression by binding to the mSin3/histone deacetylase (HDAC) transcriptional repressor complex. In the present study, we show that BRMS1 is a novel substrate of Cyclin-Dependent Kinase 2 (CDK2) that is phosphorylated on serine 237 (S237). Although CDKs are known to regulate cell cycle progression, the mutation of BRMS1 on serine 237 did not affect cell cycle progression and proliferation of MDA-MB-231 breast cancer cells; however, their migration was affected. Phosphorylation of BRMS1 does not affect its association with the mSin3/HDAC transcriptional repressor complex or its transcriptional repressor activity. The serine 237 phosphorylation site is immediately proximal to a C-terminal nuclear localization sequence that plays an important role in BRMS1-mediated metastasis suppression but phosphorylation does not control BRMS1 subcellular localization. Our studies demonstrate that CDK-mediated phosphorylation of BRMS1 regulates the migration of tumor cells