دورية أكاديمية
أعرض في EDS

Interactions between cancer cells and immune cells drive transitions to mesenchymal-like states in glioblastoma.

التفاصيل البيبلوغرافية
العنوان: Interactions between cancer cells and immune cells drive transitions to mesenchymal-like states in glioblastoma.
المؤلفون: Hara T; Department of Pathology and Center for Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA; Klarman Cell Observatory, Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA; Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA; Laboratory of Genetics, Salk Institute for Biological Studies, La Jolla, CA 92037, USA., Chanoch-Myers R; Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 761001, Israel., Mathewson ND; Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA; Department of Cancer Immunology and Virology, Department of Microbiology and Immunobiology, Department of Neurology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02215, USA., Myskiw C; Laboratory of Genetics, Salk Institute for Biological Studies, La Jolla, CA 92037, USA., Atta L; Department of Biomedical Engineering, Johns Hopkins University, Baltimore, MD 21218, USA., Bussema L; Department of Pathology and Center for Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA; Klarman Cell Observatory, Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA; Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA., Eichhorn SW; Howard Hughes Medical Institute, Harvard University, Cambridge, MA 02138, USA; Department of Chemistry and Chemical Biology, Department of Physics, Harvard University, Cambridge, MA 02138, USA., Greenwald AC; Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 761001, Israel., Kinker GS; Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 761001, Israel; Department of Physiology, Institute of Bioscience, University of Sao Paulo, Sao Paulo, Brazil., Rodman C; Department of Pathology and Center for Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA., Gonzalez Castro LN; Department of Pathology and Center for Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA; Klarman Cell Observatory, Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA; Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA; Department of Neurology and Center for Neuro-Oncology, Brigham and Women's - Dana-Farber Cancer Center and Harvard Medical School, Boston, MA 02115, USA., Wakimoto H; Department of Neurosurgery, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA., Rozenblatt-Rosen O; Klarman Cell Observatory, Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA; Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA., Zhuang X; Howard Hughes Medical Institute, Harvard University, Cambridge, MA 02138, USA; Department of Chemistry and Chemical Biology, Department of Physics, Harvard University, Cambridge, MA 02138, USA., Fan J; Department of Biomedical Engineering, Johns Hopkins University, Baltimore, MD 21218, USA., Hunter T; Laboratory of Genetics, Salk Institute for Biological Studies, La Jolla, CA 92037, USA., Verma IM; Laboratory of Genetics, Salk Institute for Biological Studies, La Jolla, CA 92037, USA., Wucherpfennig KW; Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA; Department of Cancer Immunology and Virology, Department of Microbiology and Immunobiology, Department of Neurology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02215, USA., Regev A; Klarman Cell Observatory, Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA; Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA; Howard Hughes Medical Institute, Koch Institute for Integrative Cancer Research, Department of Biology, MIT, Cambridge, MA 02139, USA., Suvà ML; Department of Pathology and Center for Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA; Klarman Cell Observatory, Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA; Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA. Electronic address: suva.mario@mgh.harvard.edu., Tirosh I; Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 761001, Israel. Electronic address: itayt@weizmann.ac.il.
المصدر: Cancer cell [Cancer Cell] 2021 Jun 14; Vol. 39 (6), pp. 779-792.e11. Date of Electronic Publication: 2021 Jun 03.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Cell Press Country of Publication: United States NLM ID: 101130617 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1878-3686 (Electronic) Linking ISSN: 15356108 NLM ISO Abbreviation: Cancer Cell Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Cambridge, Mass. : Cell Press, c2002-
مواضيع طبية MeSH: Brain Neoplasms/*immunology , Brain Neoplasms/*pathology , Glioblastoma/*immunology , Glioblastoma/*pathology , T-Lymphocytes/*immunology , Tumor-Associated Macrophages/*immunology, Animals ; Brain Neoplasms/genetics ; Cells, Cultured ; Cytokine Receptor gp130/genetics ; Cytokine Receptor gp130/metabolism ; Cytotoxicity, Immunologic ; Gene Expression Regulation, Neoplastic ; Glioblastoma/genetics ; Humans ; Leukemia Inhibitory Factor Receptor alpha Subunit/genetics ; Leukemia Inhibitory Factor Receptor alpha Subunit/metabolism ; Mice, Inbred C57BL ; Mice, Transgenic ; Oncostatin M/metabolism ; Oncostatin M Receptor beta Subunit/genetics ; Oncostatin M Receptor beta Subunit/metabolism ; STAT3 Transcription Factor/genetics ; STAT3 Transcription Factor/metabolism ; Tumor Microenvironment ; Tumor-Associated Macrophages/pathology ; Mice
مستخلص: The mesenchymal subtype of glioblastoma is thought to be determined by both cancer cell-intrinsic alterations and extrinsic cellular interactions, but remains poorly understood. Here, we dissect glioblastoma-to-microenvironment interactions by single-cell RNA sequencing analysis of human tumors and model systems, combined with functional experiments. We demonstrate that macrophages induce a transition of glioblastoma cells into mesenchymal-like (MES-like) states. This effect is mediated, both in vitro and in vivo, by macrophage-derived oncostatin M (OSM) that interacts with its receptors (OSMR or LIFR) in complex with GP130 on glioblastoma cells and activates STAT3. We show that MES-like glioblastoma states are also associated with increased expression of a mesenchymal program in macrophages and with increased cytotoxicity of T cells, highlighting extensive alterations of the immune microenvironment with potential therapeutic implications.
Competing Interests: Declaration of interests M.L.S. and K.W.W. are equity holders, scientific co-founders, and advisory board members of Immunitas Therapeutics. I.T. is advisory board member of Immunitas Therapeutics. A.R. is a founder and equity holder of Celsius Therapeutics, an equity holder in Immunitas Therapeutics, and until July 31, 2020, was an SAB member for Thermo Fisher Scientific, Syros Pharmaceuticals, Asimov and Neogene Therapeutics. O.R.R. and A.R. are employees of Genentech since October 19, 2020, and August 1, 2020, respectively. K.W.W. serves on the scientific advisory board of TCR2 Therapeutics, T-Scan Therapeutics, SQZ Biotech, and Nextechinvest, and receives sponsored research funding from Novartis. N.D.M. serves as a scientific advisor to Immunitas Therapeutics. X.Z. is a co-founder and consultant for Vizgen, Inc.
(Copyright © 2021 Elsevier Inc. All rights reserved.)
التعليقات: Comment in: Cancer Cell. 2021 Jun 14;39(6):743-745. (PMID: 34087163)
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معلومات مُعتمدة: R37 CA245523 United States CA NCI NIH HHS; United States HHMI Howard Hughes Medical Institute; K12 CA090354 United States CA NCI NIH HHS; R01 CA195613 United States CA NCI NIH HHS; L30 CA231679 United States CA NCI NIH HHS; P50 CA165962 United States CA NCI NIH HHS; P30 CA014195 United States CA NCI NIH HHS
فهرسة مساهمة: Keywords: GBM; OSM; glioblastoma; macrophage; mesenchymal; scRNA-seq; tumor microenvironment
المشرفين على المادة: 0 (IL6ST protein, human)
0 (LIFR protein, human)
0 (Leukemia Inhibitory Factor Receptor alpha Subunit)
0 (OSMR protein, human)
0 (Oncostatin M Receptor beta Subunit)
0 (STAT3 Transcription Factor)
0 (STAT3 protein, human)
106956-32-5 (Oncostatin M)
133483-10-0 (Cytokine Receptor gp130)
تواريخ الأحداث: Date Created: 20210604 Date Completed: 20211217 Latest Revision: 20240226
رمز التحديث: 20240226
مُعرف محوري في PubMed: PMC8366750
DOI: 10.1016/j.ccell.2021.05.002
PMID: 34087162
قاعدة البيانات: MEDLINE
الوصف
تدمد:1878-3686
DOI:10.1016/j.ccell.2021.05.002