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  • A novel Fer/FerT targeting compound selectively evokes metabolic stress and necrotic death in malignant cellsDisruption of the reprogrammed energy management system of malignant cells is a prioritized goal of targeted cancer therapy. Two regulators of this system are the Fer kinase, and its cancer cell specific variant, FerT, both residing in subcellular compartments including the mitochondrial electron transport chain. Here, we show that a newly developed inhibitor of Fer and FerT, E260, selectively evokes metabolic stress in cancer cells by imposing mitochondrial dysfunction and deformation, and onset of energy-consuming autophagy which decreases the cellular ATP level. Notably, Fer was also found to associate with PARP-1 and E260 disrupted this association thereby leading to PARP-1 activation. The cooperative intervention with these metabolic pathways leads to energy crisis and necrotic death in malignant, but not in normal human cells, and to the suppression of tumors growth in vivo. Thus, E260 is a new anti-cancer agent which imposes metabolic stress and cellular death in cancer cells.
  • Multifunctional nanoparticles as a tissue adhesive and an injectable marker for image-guided procedures组织粘合剂作为缝合和钉扎的一种替代品,用于外科手术或创伤后伤口闭合和损伤组织的重新连接。由于这些粘合剂的方便性和有效性,特别是在微创手术中,这些粘合剂受到越来越多的关注。
  • PTEN counteracts FBXL2 to promote IP3R3- and Ca2+-mediated apoptosis limiting tumour growthIn response to environmental cues that promote IP3 (inositol 1,4,5-trisphosphate) generation, IP3 receptors (IP3Rs) located on the endoplasmic reticulum allow the ‘quasisynaptical’ feeding of calcium to the mitochondria to promote oxidative phosphorylation1. However, persistent Ca2+ release results in mitochondrial Ca2+ overload and consequent apoptosis2. Among the three mammalian IP3Rs, IP3R3 appears to be the major player in Ca2+-dependent apoptosis. Here we show that the F-box protein FBXL2 (the receptor subunit of one of 69 human SCF (SKP1, CUL1, F-box protein) ubiquitin ligase complexes3) binds IP3R3 and targets it for ubiquitin-, p97- and proteasome-mediated degradation to limit Ca2+ influx into mitochondria.
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厦门大学分子影像暨转化医学研究中心 福建省分子影像诊疗工程技术研究中心 厦门市分子影像工程技术研究中心 版权所有
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