دورية أكاديمية
أعرض في EDS

The crosstalk between macrophages and cancer cells potentiates pancreatic cancer cachexia.

التفاصيل البيبلوغرافية
العنوان: The crosstalk between macrophages and cancer cells potentiates pancreatic cancer cachexia.
المؤلفون: Liu M; Department of Medicine, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA; Department of Surgery, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA., Ren Y; Department of Medicine, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA; Department of Surgery, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA., Zhou Z; Department of Medicine, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA; Department of Surgery, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA., Yang J; Department of Medicine, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA; Department of Surgery, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA., Shi X; Department of Medicine, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA; Department of Surgery, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA., Cai Y; Department of Medicine, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA; Department of Surgery, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA., Arreola AX; Department of Medicine, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA; Department of Pathology, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA., Luo W; Department of Pathology, Yale School of Medicine, New Haven, CT 06519, USA., Fung KM; Department of Pathology, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA., Xu C; Department of Biostatistics and Epidemiology, Hudson College of Public Health, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA., Nipp RD; Department of Medicine, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA., Bronze MS; Department of Medicine, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA., Zheng L; Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA., Li YP; Department of Integrative Biology & Pharmacology, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA., Houchen CW; Department of Medicine, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA., Zhang Y; Department of Medicine, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA; Department of Surgery, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA. Electronic address: Yuqing-Zhang@ouhsc.edu., Li M; Department of Medicine, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA; Department of Surgery, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA. Electronic address: Min-Li@ouhsc.edu.
المصدر: Cancer cell [Cancer Cell] 2024 May 13; Vol. 42 (5), pp. 885-903.e4. Date of Electronic Publication: 2024 Apr 11.
نوع المنشور: Journal Article
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: Cachexia*/metabolism , Cachexia*/etiology , Cachexia*/pathology , Pancreatic Neoplasms*/metabolism , Pancreatic Neoplasms*/pathology , Pancreatic Neoplasms*/complications , Cytokine TWEAK*/metabolism , Macrophages*/metabolism, Animals ; Humans ; Mice ; NF-kappa B/metabolism ; Cell Line, Tumor ; Tumor Microenvironment ; Muscular Atrophy/metabolism ; Muscular Atrophy/etiology ; Muscular Atrophy/pathology ; Chemokine CCL5/metabolism ; Signal Transduction ; TNF Receptor-Associated Factor 6/metabolism ; Tumor Necrosis Factors/metabolism ; Receptors, CCR2/metabolism ; Chemokine CCL2/metabolism ; Mice, Inbred C57BL
مستخلص: With limited treatment options, cachexia remains a major challenge for patients with cancer. Characterizing the interplay between tumor cells and the immune microenvironment may help identify potential therapeutic targets for cancer cachexia. Herein, we investigate the critical role of macrophages in potentiating pancreatic cancer induced muscle wasting via promoting TWEAK (TNF-like weak inducer of apoptosis) secretion from the tumor. Specifically, depletion of macrophages reverses muscle degradation induced by tumor cells. Macrophages induce non-autonomous secretion of TWEAK through CCL5/TRAF6/NF-κB pathway. TWEAK promotes muscle atrophy by activating MuRF1 initiated muscle remodeling. Notably, tumor cells recruit and reprogram macrophages via the CCL2/CCR2 axis and disrupting the interplay between macrophages and tumor cells attenuates muscle wasting. Collectively, this study identifies a feedforward loop between pancreatic cancer cells and macrophages, underlying the non-autonomous activation of TWEAK secretion from tumor cells thereby providing promising therapeutic targets for pancreatic cancer cachexia.
Competing Interests: Declaration of interests C.W. Houchen has ownership interest in COARE Holdings Inc.
(Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)
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معلومات مُعتمدة: R01 CA186338 United States CA NCI NIH HHS; R01 CA203108 United States CA NCI NIH HHS; R01 CA247234 United States CA NCI NIH HHS
فهرسة مساهمة: Keywords: CCL2; CCL5; RELB; TWEAK; cancer cachexia; macrophages; metabolic reprogramming; muscle wasting; p65; tumor microenvironment
تواريخ الأحداث: Date Created: 20240412 Date Completed: 20240514 Latest Revision: 20240611
رمز التحديث: 20240611
مُعرف محوري في PubMed: PMC11162958
DOI: 10.1016/j.ccell.2024.03.009
PMID: 38608702
قاعدة البيانات: MEDLINE
الوصف
تدمد:1878-3686
DOI:10.1016/j.ccell.2024.03.009