![]() ![]() ![]() Correlations between G-CSF/G- CSFR and clinical characteristics, VEGF-A levels and overall survival were analyzed. A total of 40 paired GC tissues and matched adjacent mucosa were used to measure the G-CSF and G- CSFR levels by ELISA. MATERIAL AND METHODS Seventy GC tissue samples were collected for G-CSF and G- CSFR detection by immunohistochemistry. However, the effects of G-CSF and G- CSFR expression on GC patient survival remain unclear. Thus, G-CSF might be a potential tumor marker. Granulocyte colony-stimulating factor (G-CSF) promotes tumor growth and angiogenesis, which can be minimized with the anti-G-CSF antibody. Although adding anti-angiogenic drugs to chemotherapy improves patient survival slightly, identifying anti-angiogenic therapy-sensitive patients remains challenging for oncologists. Highly Expressed Granulocyte Colony-Stimulating Factor (G-CSF) and Granulocyte Colony-Stimulating Factor Receptor (G- CSFR) in Human Gastric Cancer Leads to Poor Survival.įan, Zhisong Li, Yong Zhao, Qun Fan, Liqiao Tan, Bibo Zuo, Jing Hua, Kelei Ji, QiangīACKGROUND Chemotherapy for advanced gastric cancer (GC) patients has been the mainstay of therapy for many years. We propose that signaling pathways activated by tyrosine kinase receptors may regulate erythroid potential and commitment decisions in multipotent progenitor cells and that PLC may play a key role in this process. Furthermore, phospholipase C (PLC) inhibitor U73122 interfered with the negative effects of ligand-activated murine M-CSFR on EML cell erythroid potential. Using chimeric receptors between human and murine M-CSFR, we showed that the effects of M-CSF on EML cell differentiation potential are mediated by a large region in the intracellular domain of murine M-CSFR. In contrast, EML cells expressing human M-CSFR proliferated in response to M-CSF without any changes in erythroid or myeloid potential. EML cells transduced with murine M-CSFR proliferated in response to M-CSF but also exhibited a sharp and rapid decrease in BFU-E frequency associated with an increase in CFU-GM frequency. ![]() Effects of specific inhibitors of signaling molecules were investigated. We determined BFU-E and CFU-GM frequencies among EML cells transduced with murine M-CSFR, human M-CSFR, or chimeric receptors, and cultivated in the presence of SCF, M-CSF, or both growth factors. EML cells are stem cell factor (SCF)-dependent murine cells that give rise spontaneously to pre-B cells, burst-forming unit erythroid (BFU-E), and colony-forming unit granulocyte macrophage (CFU-GM). To test the hypothesis that hematopoietic growth factors may influence lineage choice in pluripotent progenitor cells, we investigated the effects of macrophage colony-stimulating factor ( M-CSF) on erythroid and myeloid potentials of multipotent EML cells ectopically expressing M-CSF receptor ( M-CSFR). Pawlak, G Grasset, M F Arnaud, S Blanchet, J P Mouchiroud, G Competence is thus shown to be under direct nutritional control by a fructose-specific PTS.Receptor for macrophage colony-stimulating factor transduces a signal decreasing erythroid potential in the multipotent hematopoietic EML cell line. Development of competence under standard inducing conditions was reduced 250-fold by the ptsI mutation, unless cells were provided with exogenous cAMP. In wild-type cells the non-metabolizable fructose analogue xylitol prevented fermentation of these sugars, confirming that the fructose PTS regulates cAMP levels. The ptsI mutation also prevented fermentation of ribose and galactose, but utilization of these cAMP-dependent sugars was restored by addition of cAMP. A ptsI null mutation reduced fructose uptake to 1% of the wild-type rate, and abolished fructose fermentation even when exogenous cAMP was provided. In vitro phosphorylation assays confirmed the presence of functional PTS components. influenzae ptsI gene, encoding PTS Enzyme I genome analysis locates it in a pts operon structurally homologous to those of enteric bacteria. We have demonstrated the existence of a simple PTS in H. In enteric bacteria, cAMP levels are controlled by the phosphoenolpyruvate:glycose phosphotransferase system (PTS) in response to changes in availability of the preferred sugars it transports. Changes in intracellular cAMP concentration play important roles in Haemophilus influenzae, regulating both sugar utilization and competence for natural transformation. ![]()
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