Complement pathway activation mediates pancreatic cancer–induced muscle wasting and pathological remodeling
Cancer cachexia is a multifactorial condition characterized by skeletal muscle wasting that impairs quality of life and longevity for many cancer patients. A greater understanding of the molecular etiology of this condition is needed for effective therapies to be developed. We performed a quantitati...
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| Vydané v: | The Journal of clinical investigation Ročník 135; číslo 12 |
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| Hlavní autori: | , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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United States
American Society for Clinical Investigation
30.06.2025
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| ISSN: | 1558-8238, 0021-9738, 1558-8238 |
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| Abstract | Cancer cachexia is a multifactorial condition characterized by skeletal muscle wasting that impairs quality of life and longevity for many cancer patients. A greater understanding of the molecular etiology of this condition is needed for effective therapies to be developed. We performed a quantitative proteomic analysis of skeletal muscle from cachectic pancreatic ductal adenocarcinoma (PDAC) patients and non-cancer controls, followed by immunohistochemical analyses of muscle cross sections. These data provide evidence of a local inflammatory response in muscles of cachectic PDAC patients, including an accumulation of plasma proteins and recruitment of immune cells into muscle that may promote the pathological remodeling of muscle. Our data further support the complement system as a potential mediator of these processes, which we tested by injecting murine pancreatic cancer cells into wild-type mice and mice with genetic deletion of the central complement component 3 (C3-/- mice). Compared with wild-type mice, C3-/- mice showed attenuated tumor-induced muscle wasting and dysfunction and reduced immune cell recruitment and fibrotic remodeling of muscle. These studies demonstrate that complement activation contributes to the skeletal muscle pathology and dysfunction in PDAC, suggesting that the complement system may possess therapeutic potential in preserving skeletal muscle mass and function. |
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| AbstractList | Cancer cachexia is a multifactorial condition characterized by skeletal muscle wasting that impairs quality of life and longevity for many cancer patients. A greater understanding of the molecular etiology of this condition is needed for effective therapies to be developed. We performed a quantitative proteomic analysis of skeletal muscle from cachectic pancreatic ductal adenocarcinoma (PDAC) patients and non-cancer controls, followed by immunohistochemical analyses of muscle cross sections. These data provide evidence of a local inflammatory response in muscles of cachectic PDAC patients, including an accumulation of plasma proteins and recruitment of immune cells into muscle that may promote the pathological remodeling of muscle. Our data further support the complement system as a potential mediator of these processes, which we tested by injecting murine pancreatic cancer cells into wild-type mice and mice with genetic deletion of the central complement component 3 (C3-/- mice). Compared with wild-type mice, C3-/- mice showed attenuated tumor-induced muscle wasting and dysfunction and reduced immune cell recruitment and fibrotic remodeling of muscle. These studies demonstrate that complement activation contributes to the skeletal muscle pathology and dysfunction in PDAC, suggesting that the complement system may possess therapeutic potential in preserving skeletal muscle mass and function. Cancer cachexia is a multifactorial condition characterized by skeletal muscle wasting that impairs quality of life and longevity for many cancer patients. A greater understanding of the molecular etiology of this condition is needed for effective therapies to be developed. We performed a quantitative proteomic analysis of skeletal muscle from cachectic pancreatic ductal adenocarcinoma (PDAC) patients and non-cancer controls, followed by immunohistochemical analyses of muscle cross sections. These data provide evidence of a local inflammatory response in muscles of cachectic PDAC patients, including an accumulation of plasma proteins and recruitment of immune cells into muscle that may promote the pathological remodeling of muscle. Our data further support the complement system as a potential mediator of these processes, which we tested by injecting murine pancreatic cancer cells into wild-type mice and mice with genetic deletion of the central complement component 3 ([C3.sup.-/-] mice). Compared with wild-type mice, [C3.sup.- /-] mice showed attenuated tumor-induced muscle wasting and dysfunction and reduced immune cell recruitment and fibrotic remodeling of muscle. These studies demonstrate that complement activation contributes to the skeletal muscle pathology and dysfunction in PDAC, suggesting that the complement system may possess therapeutic potential in preserving skeletal muscle mass and function. Cancer cachexia is a multifactorial condition characterized by skeletal muscle wasting that impairs quality of life and longevity for many cancer patients. A greater understanding of the molecular etiology of this condition is needed for effective therapies to be developed. We performed a quantitative proteomic analysis of skeletal muscle from cachectic pancreatic ductal adenocarcinoma (PDAC) patients and non-cancer controls, followed by immunohistochemical analyses of muscle cross sections. These data provide evidence of a local inflammatory response in muscles of cachectic PDAC patients, including an accumulation of plasma proteins and recruitment of immune cells into muscle that may promote the pathological remodeling of muscle. Our data further support the complement system as a potential mediator of these processes, which we tested by injecting murine pancreatic cancer cells into wild-type mice and mice with genetic deletion of the central complement component 3 (C3–/– mice). Compared with wild-type mice, C3–/– mice showed attenuated tumor-induced muscle wasting and dysfunction and reduced immune cell recruitment and fibrotic remodeling of muscle. These studies demonstrate that complement activation contributes to the skeletal muscle pathology and dysfunction in PDAC, suggesting that the complement system may possess therapeutic potential in preserving skeletal muscle mass and function. Complement system activation plays a major role in pancreatic cancer cachexia, which was informed from proteomic analysis of skeletal muscle from pancreatic cancer patients. Cancer cachexia is a multifactorial condition characterized by skeletal muscle wasting that impairs quality of life and longevity for many cancer patients. A greater understanding of the molecular etiology of this condition is needed for effective therapies to be developed. We performed a quantitative proteomic analysis of skeletal muscle from cachectic pancreatic ductal adenocarcinoma (PDAC) patients and non-cancer controls, followed by immunohistochemical analyses of muscle cross-sections. These data provide evidence of a local inflammatory response in muscles of cachectic PDAC patients, including an accumulation of plasma proteins and recruitment of immune cells into muscle that may promote the pathological remodeling of muscle. Our data further support the complement system as a potential mediator of these processes, which we tested by injecting murine pancreatic cancer cells into wild type (WT) mice, or mice with genetic deletion of the central complement component 3 (C3-/- mice). Compared to WT mice, C3-/- mice showed attenuated tumor-induced muscle wasting and dysfunction and reduced immune cell recruitment and fibrotic remodeling of muscle. These studies demonstrate that complement activation is contributory to the skeletal muscle pathology and dysfunction in PDAC, suggesting that the complement system may possess therapeutic potential in preserving skeletal muscle mass and function.Cancer cachexia is a multifactorial condition characterized by skeletal muscle wasting that impairs quality of life and longevity for many cancer patients. A greater understanding of the molecular etiology of this condition is needed for effective therapies to be developed. We performed a quantitative proteomic analysis of skeletal muscle from cachectic pancreatic ductal adenocarcinoma (PDAC) patients and non-cancer controls, followed by immunohistochemical analyses of muscle cross-sections. These data provide evidence of a local inflammatory response in muscles of cachectic PDAC patients, including an accumulation of plasma proteins and recruitment of immune cells into muscle that may promote the pathological remodeling of muscle. Our data further support the complement system as a potential mediator of these processes, which we tested by injecting murine pancreatic cancer cells into wild type (WT) mice, or mice with genetic deletion of the central complement component 3 (C3-/- mice). Compared to WT mice, C3-/- mice showed attenuated tumor-induced muscle wasting and dysfunction and reduced immune cell recruitment and fibrotic remodeling of muscle. These studies demonstrate that complement activation is contributory to the skeletal muscle pathology and dysfunction in PDAC, suggesting that the complement system may possess therapeutic potential in preserving skeletal muscle mass and function. |
| Audience | Academic |
| Author | Atkinson, Carl Ducharme, Jeremy B. Callaway, Chandler S. Trevino, Jose G. Judge, Sarah M. Judge, Andrew R. D’Lugos, Andrew C. |
| AuthorAffiliation | 4 Department of Surgery, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA 2 Myology Institute, University of Florida, Gainesville, Florida, USA 1 Department of Physical Therapy and 3 University of Florida Health Cancer Center, Gainesville, Florida, USA 5 Division of Pulmonary Medicine, University of Florida, Gainesville, Florida, USA |
| AuthorAffiliation_xml | – name: 3 University of Florida Health Cancer Center, Gainesville, Florida, USA – name: 2 Myology Institute, University of Florida, Gainesville, Florida, USA – name: 5 Division of Pulmonary Medicine, University of Florida, Gainesville, Florida, USA – name: 4 Department of Surgery, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA – name: 1 Department of Physical Therapy and |
| Author_xml | – sequence: 1 givenname: Andrew C. surname: D’Lugos fullname: D’Lugos, Andrew C. – sequence: 2 givenname: Jeremy B. surname: Ducharme fullname: Ducharme, Jeremy B. – sequence: 3 givenname: Chandler S. surname: Callaway fullname: Callaway, Chandler S. – sequence: 4 givenname: Jose G. surname: Trevino fullname: Trevino, Jose G. – sequence: 5 givenname: Carl surname: Atkinson fullname: Atkinson, Carl – sequence: 6 givenname: Sarah M. surname: Judge fullname: Judge, Sarah M. – sequence: 7 givenname: Andrew R. orcidid: 0000-0002-4488-291X surname: Judge fullname: Judge, Andrew R. |
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| Keywords | Oncology Muscle Muscle biology Proteomics Cancer |
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| SubjectTerms | Animals Cachexia - etiology Cachexia - genetics Cachexia - immunology Cachexia - metabolism Cachexia - pathology Carcinoma, Pancreatic Ductal - complications Carcinoma, Pancreatic Ductal - genetics Carcinoma, Pancreatic Ductal - immunology Carcinoma, Pancreatic Ductal - metabolism Carcinoma, Pancreatic Ductal - pathology Causes of Cell Line, Tumor Complement Activation Complement C3 - deficiency Complement C3 - genetics Complement C3 - immunology Complement C3 - metabolism Female Health aspects Humans Male Mice Mice, Knockout Muscle biology Muscle diseases Muscle, Skeletal - immunology Muscle, Skeletal - metabolism Muscle, Skeletal - pathology Muscles Muscular Atrophy - etiology Muscular Atrophy - genetics Muscular Atrophy - immunology Muscular Atrophy - pathology Oncology Pancreatic cancer Pancreatic Neoplasms - complications Pancreatic Neoplasms - genetics Pancreatic Neoplasms - immunology Pancreatic Neoplasms - metabolism Pancreatic Neoplasms - pathology Physiological aspects |
| Title | Complement pathway activation mediates pancreatic cancer–induced muscle wasting and pathological remodeling |
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