Publications by authors named "Maithao N Le"
The goal of this study was to examine the effects of metabotropic glutamate receptor-1 (GRM1) blockade on melanoma anchorage-independent growth and invasion. We performed colony and invasion assays using GRM1-expressing melanoma lines and the GRM1-negative UACC930 line. Using the glutamate-release inhibitor Riluzole or the non-competitive GRM1 antagonist BAY 36-7620 we were able to induce considerable inhibition of colony formation and invasion in GRM1-expressing melanoma lines.
View Article and Find Full Text PDFPurpose: Ectopic expression of GRM1 in murine melanocytes results in transformation into a form of melanoma, and more than 60% of human melanoma samples tested ectopically express GRM1. Stimulation of this receptor in vitro results in up-regulation of activated extracellular signal-regulated kinase (ERK). Furthermore, a xenograft model of melanoma treated with riluzole, an oral GRM1 blocking agent, showed decreased tumor growth compared with the untreated controls.
View Article and Find Full Text PDFArticle Synopsis
- Insulin activates Stat5 in cells with high insulin receptor (IR) levels, indicating a potential role for Stat5 in insulin signaling pathways.
- The interaction between Stat5b and insulin receptor substrate 1 (IRS-1) occurs at a specific phosphorylation site on the IR, and this interaction is crucial for Stat5 activation.
- While JAK kinases also play a role in Stat5 activation after insulin stimulation, some pathways appear to be JAK-independent, suggesting that the IR can directly phosphorylate Stat5b.