Impact of bee venom and melittin on apoptosis and biotransformation in colorectal carcinoma cell lines

© 2019, © 2019 Informa UK Limited, trading as Taylor & Francis Group. This study provides data about anticancer properties of bee venom and its dominant compound, melittin on colorectal carcinoma cells (HCT-116 and SW-480) in regard to their proapoptotic activity and expression of genes involved in biotransformation process. Based on results, they are strong cytotoxins, where the melittin showed also selectivity against cancer cells compared to normal, HaCat. They induce proapoptotic activity by affecting apoptosis signaling molecules (Fas receptors, caspase 9, and members of Bcl-2 family of proteins) and mainly suppress expression of genes involved in their biotransformation, suggesting their ability to develop the resistance of colorectal cancer cells

MIF is a noncognate ligand of CXC chemokine receptors in inflammatory and atherogenic cell recruitment

© 2007 Nature Publishing GroupThe cytokine macrophage migration inhibitory factor (MIF) plays a critical role in inflammatory diseases and atherogenesis. We identify the chemokine receptors CXCR2 and CXCR4 as functional receptors for MIF. MIF triggered G(alphai)- and integrin-dependent arrest and chemotaxis of monocytes and T cells, rapid integrin activation and calcium influx through CXCR2 or CXCR4. MIF competed with cognate ligands for CXCR4 and CXCR2 binding, and directly bound to CXCR2. CXCR2 and CD74 formed a receptor complex, and monocyte arrest elicited by MIF in inflamed or atherosclerotic arteries involved both CXCR2 and CD74. In vivo, Mif deficiency impaired monocyte adhesion to the arterial wall in atherosclerosis-prone mice, and MIF-induced leukocyte recruitment required Il8rb (which encodes Cxcr2). Blockade of Mif but not of canonical ligands of Cxcr2 or Cxcr4 in mice with advanced atherosclerosis led to plaque regression and reduced monocyte and T-cell content in plaques. By activating both CXCR2 and CXCR4, MIF displays chemokine-like functions and acts as a major regulator of inflammatory cell recruitment and atherogenesis. Targeting MIF in individuals with manifest atherosclerosis can potentially be used to treat this condition.Jürgen Bernhagen, Regina Krohn, Hongqi Lue, Julia L Gregory, Alma Zernecke, Rory R Koenen, Manfred Dewor, Ivan Georgiev, Andreas Schober, Lin Leng, Teake Kooistra, Günter Fingerle-Rowson, Pietro Ghezzi, Robert Kleemann, Shaun R McColl, Richard Bucala, Michael J Hickey & Christian Webe