Intestinal Cell News 4.11 March 23, 2018 | |
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TOP STORYResearchers showed that NF-κB1 deficiency, even loss of a single allele, resulted in spontaneous invasive gastric cancer in mice that mirrored the histopathological progression of human intestinal-type gastric adenocarcinoma. [Immunity] Abstract | Graphical Abstract | |
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PUBLICATIONS(Ranked by impact factor of the journal)Wnt Ligands Influence Tumor Initiation by Controlling the Number of Intestinal Stem Cells Reduction of Wnt ligand secretion accelerates fixation of Apc-deficient cells within the crypt leading to accelerated tumorigenesis. Therefore, ligand-based Wnt signaling influenced the number of stem cells, fixation speed of Apc mutations and the speed and likelihood of adenoma formation. [Nat Commun] Full Article Scientists investigated both the source and the functional role of stromal Wnts and Wnts and R-spondin (RSPO) in regulation of intestinal homeostasis. RSPO3 was highly expressed in pericryptal myofibroblasts in the lamina propria and is several orders of magnitude more potent than RSPO1 in stimulating both Wnt/β-catenin signaling and organoid growth. [Proc Natl Acad Sci USA] Full Article Multivariate analysis showed that colorectal cancer (CRC) patients with CREPT protein overexpression were significantly associated with poor disease-free survival. CREPT significantly accelerated CRC cell proliferation and metastasis both in vitro and in vivo. [Oncogene] Full Article Using human colorectal cancer (CRC) cells harboring different Wnt/β-catenin pathway mutations in APC/KRAS or β-catenin/KRAS genes, and both genetic and pharmacological knockdown approaches, the authors showed that oncogenic β-catenin signaling negatively regulates the expression of Na+/H+ exchanger 3 regulating factor 1 (NHERF1), a PDZ-adaptor protein that is usually lost or downregulated in early dysplastic adenomas to exacerbate nuclear β-catenin activity. [Oncogene] Full Article The Intestinal Stem Cell Regulating Gene ASCL2 Is Required for L1-Mediated Colon Cancer Progression In L1 overexpressing colorectal cancer (CRC) cells scientists found an increase in ASCL2, a decrease in E-cadherin and accumulation of nuclear β-catenin, β-catenin-LEF1/TCF transactivation and target gene expression. [Cancer Lett] Abstract Investigators observed that nuclear receptor binding protein 1 (NRBP1) expression levels were significantly reduced in colorectal cancer (CRC) tissues compared with corresponding adjacent normal tissues, and high NRBP1 expression correlated with better prognosis in CRC. Overexpression of NRBP1 inhibited CRC cell proliferation and promoted apoptosis in vitro and in vivo. [Cell Death Dis] Full Article Researchers evaluated the molecular mechanisms regulating the effects of nucleotides on weaning. Nucleotide treatment induced trefoil factor 3 (TFF3) expression and IPEC-J2 cell growth and reduced wound width. Treatment with nucleosides and TFF3 in lipopolysaccharide-challenged IPEC-J2 cells increased intestinal transepithelial electrical resistance and decreased intestinal permeability. [Sci Rep] Full Article Colon cancer cells without cartilage oligomeric matrix protein were defective with respect to the ability to proliferate, colony formation, the ability to resist 5-fluorouracil-induced apoptosis and the growth of xenograft tumors in mice. [J Cancer Res Clin Oncol] Abstract | |
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REVIEWSMechanisms for Intestinal Regeneration Scientists summarize the notable structures and pathways in intestinal epithelial growth before presenting the current main areas of active research in intestinal regeneration. [Curr Opin Pediatr] Abstract Visit our reviews page to see a complete list of reviews in the intestinal cell research field. | |
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INDUSTRY NEWSMerus N.V. and the Vall d’Hebron Institute of Oncology announced a strategic research collaboration to develop novel agents for therapeutic applications. [Merus N.V.] Press Release CGT Catapult to Support UK Network of Advanced Therapies Treatment Centers The Cell and Gene Therapy (CGT) Catapult will support three UK sites awarded funding to form a network of advanced therapies treatment centers – joint ventures set up to include industry, academic and NHS partners, and funded by Innovate UK. [The Cell and Gene Therapy Catapult] Press Release | |
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POLICY NEWSFinal 2018 Budget Deal Should Help the National Science Foundation in 2019, Too The 4% increase for the National Science Foundation (NSF) in Alexandria, Virginia, in the 2018 omnibus spending bill hammered out by congressional leaders may be modest next to what its peer science agencies received. But it does offer NSF officials more breathing room to fund some major initiatives starting next year. [ScienceInsider] Editorial Expectations Are High for UKRI, the United Kingdom’s New £6 Billion Research Behemoth Combine U.S. agencies akin to the National Institutes of Health, National Science Foundation, and National Endowment for the Humanities. Toss in some energy and innovation research and fuel it all with the largest boost in R&D spending in recent history. Then put one person in charge. [ScienceInsider] Editorial HIV Researcher Is New Head of US Public-Health Agency HIV researcher Robert Redfield will lead the Centers for Disease Control and Prevention, Secretary of Health and Human Services Alex Azar announced. [Nature News] Editorial
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EVENTSNEW Gordon Research Conferences: Cell Death Visit our events page to see a complete list of events in the community.
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JOB OPPORTUNITIESNEW Postdoctoral Fellowship – Intestinal Cancer (University of Gothenburg) Postdoctoral Research Fellow – Colon Cancer (Health Sciences North Research Institute) Director Position – Immune Intestinal Homeostasis (Institute for Basic Science) Postdoctoral Fellow – Mucosal Immunology (Centre of Molecular Inflammation Research) Postdoctoral Fellow – Inflammatory Bowel Disease (Marshall University) Postdoctoral Fellow – Cancer Biology (Johns Hopkins University) Postdoctoral Fellow – Cancer Biology (University of Arkansas for Medical Science) Recruit Top Talent: Reach potential candidates by posting your organization’s career opportunities on the Connexon Creative Job Board at no cost.
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