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The crosstalk between macrophages and cancer cells potentiates pancreatic cancer cachexia.
Liu, Mingyang; Ren, Yu; Zhou, Zhijun; Yang, Jingxuan; Shi, Xiuhui; Cai, Yang; Arreola, Alex X; Luo, Wenyi; Fung, Kar-Ming; Xu, Chao; Nipp, Ryan D; Bronze, Michael S; Zheng, Lei; Li, Yi-Ping; Houchen, Courtney W; Zhang, Yuqing; Li, Min.
Affiliation
  • 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.
Cancer Cell ; 42(5): 885-903.e4, 2024 May 13.
Article in En | MEDLINE | ID: mdl-38608702
ABSTRACT
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.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Pancreatic Neoplasms / Cachexia / Cytokine TWEAK / Macrophages Limits: Animals / Humans Language: En Journal: Cancer Cell Journal subject: NEOPLASIAS Year: 2024 Document type: Article Affiliation country: United States
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Pancreatic Neoplasms / Cachexia / Cytokine TWEAK / Macrophages Limits: Animals / Humans Language: En Journal: Cancer Cell Journal subject: NEOPLASIAS Year: 2024 Document type: Article Affiliation country: United States