Mitochondrial and sarcoplasmic reticulum abnormalities in cancer cachexia: Altered energetic efficiency?
Cachexia is a wasting condition that manifests in several types of cancer, and the main characteristic is the profound loss of muscle mass. The Yoshida AH-130 tumor model has been used and the samples have been analyzed using transmission electronic microscopy, real-time PCR and Western blot techniq...
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| Published in | Biochimica et biophysica acta Vol. 1830; no. 3; pp. 2770 - 2778 |
|---|---|
| Main Authors | , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Netherlands
Elsevier B.V
01.03.2013
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0304-4165 0006-3002 1872-8006 |
| DOI | 10.1016/j.bbagen.2012.11.009 |
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| Abstract | Cachexia is a wasting condition that manifests in several types of cancer, and the main characteristic is the profound loss of muscle mass.
The Yoshida AH-130 tumor model has been used and the samples have been analyzed using transmission electronic microscopy, real-time PCR and Western blot techniques.
Using in vivo cancer cachectic model in rats, here we show that skeletal muscle loss is accompanied by fiber morphologic alterations such as mitochondrial disruption, dilatation of sarcoplasmic reticulum and apoptotic nuclei. Analyzing the expression of some factors related to proteolytic and thermogenic processes, we observed in tumor-bearing animals an increased expression of genes involved in proteolysis such as ubiquitin ligases Muscle Ring Finger 1 (MuRF-1) and Muscle Atrophy F-box protein (MAFBx). Moreover, an overexpression of both sarco/endoplasmic Ca2+-ATPase (SERCA1) and adenine nucleotide translocator (ANT1), both factors related to cellular energetic efficiency, was observed. Tumor burden also leads to a marked decreased in muscle ATP content.
In addition to muscle proteolysis, other ATP-related pathways may have a key role in muscle wasting, both directly by increasing energetic inefficiency, and indirectly, by affecting the sarcoplasmic reticulum–mitochondrial assembly that is essential for muscle function and homeostasis.
The present study reports profound morphological changes in cancer cachectic muscle, which are visualized mainly in alterations in sarcoplasmic reticulum and mitochondria. These alterations are linked to pathways that can account for energy inefficiency associated with cancer cachexia.
► Skeletal muscle from cachectic animals showed fiber morphologic alterations. ► These alterations are mitochondrial disruption and dilatation of sarcoplasmic reticulum. ► An overexpression of both sarco/endoplasmic Ca2+-ATPase (SERCA1) and adenine nucleotide translocator (ANT1) was reported. ► Tumor burden also leads to a marked decreased in muscle ATP content. |
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| AbstractList | Cachexia is a wasting condition that manifests in several types of cancer, and the main characteristic is the profound loss of muscle mass.
The Yoshida AH-130 tumor model has been used and the samples have been analyzed using transmission electronic microscopy, real-time PCR and Western blot techniques.
Using in vivo cancer cachectic model in rats, here we show that skeletal muscle loss is accompanied by fiber morphologic alterations such as mitochondrial disruption, dilatation of sarcoplasmic reticulum and apoptotic nuclei. Analyzing the expression of some factors related to proteolytic and thermogenic processes, we observed in tumor-bearing animals an increased expression of genes involved in proteolysis such as ubiquitin ligases Muscle Ring Finger 1 (MuRF-1) and Muscle Atrophy F-box protein (MAFBx). Moreover, an overexpression of both sarco/endoplasmic Ca(2+)-ATPase (SERCA1) and adenine nucleotide translocator (ANT1), both factors related to cellular energetic efficiency, was observed. Tumor burden also leads to a marked decreased in muscle ATP content.
In addition to muscle proteolysis, other ATP-related pathways may have a key role in muscle wasting, both directly by increasing energetic inefficiency, and indirectly, by affecting the sarcoplasmic reticulum-mitochondrial assembly that is essential for muscle function and homeostasis.
The present study reports profound morphological changes in cancer cachectic muscle, which are visualized mainly in alterations in sarcoplasmic reticulum and mitochondria. These alterations are linked to pathways that can account for energy inefficiency associated with cancer cachexia. Cachexia is a wasting condition that manifests in several types of cancer, and the main characteristic is the profound loss of muscle mass. The Yoshida AH-130 tumor model has been used and the samples have been analyzed using transmission electronic microscopy, real-time PCR and Western blot techniques. Using in vivo cancer cachectic model in rats, here we show that skeletal muscle loss is accompanied by fiber morphologic alterations such as mitochondrial disruption, dilatation of sarcoplasmic reticulum and apoptotic nuclei. Analyzing the expression of some factors related to proteolytic and thermogenic processes, we observed in tumor-bearing animals an increased expression of genes involved in proteolysis such as ubiquitin ligases Muscle Ring Finger 1 (MuRF-1) and Muscle Atrophy F-box protein (MAFBx). Moreover, an overexpression of both sarco/endoplasmic Ca2+-ATPase (SERCA1) and adenine nucleotide translocator (ANT1), both factors related to cellular energetic efficiency, was observed. Tumor burden also leads to a marked decreased in muscle ATP content. In addition to muscle proteolysis, other ATP-related pathways may have a key role in muscle wasting, both directly by increasing energetic inefficiency, and indirectly, by affecting the sarcoplasmic reticulum–mitochondrial assembly that is essential for muscle function and homeostasis. The present study reports profound morphological changes in cancer cachectic muscle, which are visualized mainly in alterations in sarcoplasmic reticulum and mitochondria. These alterations are linked to pathways that can account for energy inefficiency associated with cancer cachexia. ► Skeletal muscle from cachectic animals showed fiber morphologic alterations. ► These alterations are mitochondrial disruption and dilatation of sarcoplasmic reticulum. ► An overexpression of both sarco/endoplasmic Ca2+-ATPase (SERCA1) and adenine nucleotide translocator (ANT1) was reported. ► Tumor burden also leads to a marked decreased in muscle ATP content. Cachexia is a wasting condition that manifests in several types of cancer, and the main characteristic is the profound loss of muscle mass.BACKGROUNDCachexia is a wasting condition that manifests in several types of cancer, and the main characteristic is the profound loss of muscle mass.The Yoshida AH-130 tumor model has been used and the samples have been analyzed using transmission electronic microscopy, real-time PCR and Western blot techniques.METHODSThe Yoshida AH-130 tumor model has been used and the samples have been analyzed using transmission electronic microscopy, real-time PCR and Western blot techniques.Using in vivo cancer cachectic model in rats, here we show that skeletal muscle loss is accompanied by fiber morphologic alterations such as mitochondrial disruption, dilatation of sarcoplasmic reticulum and apoptotic nuclei. Analyzing the expression of some factors related to proteolytic and thermogenic processes, we observed in tumor-bearing animals an increased expression of genes involved in proteolysis such as ubiquitin ligases Muscle Ring Finger 1 (MuRF-1) and Muscle Atrophy F-box protein (MAFBx). Moreover, an overexpression of both sarco/endoplasmic Ca(2+)-ATPase (SERCA1) and adenine nucleotide translocator (ANT1), both factors related to cellular energetic efficiency, was observed. Tumor burden also leads to a marked decreased in muscle ATP content.RESULTSUsing in vivo cancer cachectic model in rats, here we show that skeletal muscle loss is accompanied by fiber morphologic alterations such as mitochondrial disruption, dilatation of sarcoplasmic reticulum and apoptotic nuclei. Analyzing the expression of some factors related to proteolytic and thermogenic processes, we observed in tumor-bearing animals an increased expression of genes involved in proteolysis such as ubiquitin ligases Muscle Ring Finger 1 (MuRF-1) and Muscle Atrophy F-box protein (MAFBx). Moreover, an overexpression of both sarco/endoplasmic Ca(2+)-ATPase (SERCA1) and adenine nucleotide translocator (ANT1), both factors related to cellular energetic efficiency, was observed. Tumor burden also leads to a marked decreased in muscle ATP content.In addition to muscle proteolysis, other ATP-related pathways may have a key role in muscle wasting, both directly by increasing energetic inefficiency, and indirectly, by affecting the sarcoplasmic reticulum-mitochondrial assembly that is essential for muscle function and homeostasis.CONCLUSIONSIn addition to muscle proteolysis, other ATP-related pathways may have a key role in muscle wasting, both directly by increasing energetic inefficiency, and indirectly, by affecting the sarcoplasmic reticulum-mitochondrial assembly that is essential for muscle function and homeostasis.The present study reports profound morphological changes in cancer cachectic muscle, which are visualized mainly in alterations in sarcoplasmic reticulum and mitochondria. These alterations are linked to pathways that can account for energy inefficiency associated with cancer cachexia.GENERAL SIGNIFICANCEThe present study reports profound morphological changes in cancer cachectic muscle, which are visualized mainly in alterations in sarcoplasmic reticulum and mitochondria. These alterations are linked to pathways that can account for energy inefficiency associated with cancer cachexia. Cachexia is a wasting condition that manifests in several types of cancer, and the main characteristic is the profound loss of muscle mass.The Yoshida AH-130 tumor model has been used and the samples have been analyzed using transmission electronic microscopy, real-time PCR and Western blot techniques.Using in vivo cancer cachectic model in rats, here we show that skeletal muscle loss is accompanied by fiber morphologic alterations such as mitochondrial disruption, dilatation of sarcoplasmic reticulum and apoptotic nuclei. Analyzing the expression of some factors related to proteolytic and thermogenic processes, we observed in tumor-bearing animals an increased expression of genes involved in proteolysis such as ubiquitin ligases Muscle Ring Finger 1 (MuRF-1) and Muscle Atrophy F-box protein (MAFBx). Moreover, an overexpression of both sarco/endoplasmic Ca2+-ATPase (SERCA1) and adenine nucleotide translocator (ANT1), both factors related to cellular energetic efficiency, was observed. Tumor burden also leads to a marked decreased in muscle ATP content.In addition to muscle proteolysis, other ATP-related pathways may have a key role in muscle wasting, both directly by increasing energetic inefficiency, and indirectly, by affecting the sarcoplasmic reticulum–mitochondrial assembly that is essential for muscle function and homeostasis.The present study reports profound morphological changes in cancer cachectic muscle, which are visualized mainly in alterations in sarcoplasmic reticulum and mitochondria. These alterations are linked to pathways that can account for energy inefficiency associated with cancer cachexia. BACKGROUND: Cachexia is a wasting condition that manifests in several types of cancer, and the main characteristic is the profound loss of muscle mass. METHODS: The Yoshida AH-130 tumor model has been used and the samples have been analyzed using transmission electronic microscopy, real-time PCR and Western blot techniques. RESULTS: Using in vivo cancer cachectic model in rats, here we show that skeletal muscle loss is accompanied by fiber morphologic alterations such as mitochondrial disruption, dilatation of sarcoplasmic reticulum and apoptotic nuclei. Analyzing the expression of some factors related to proteolytic and thermogenic processes, we observed in tumor-bearing animals an increased expression of genes involved in proteolysis such as ubiquitin ligases Muscle Ring Finger 1 (MuRF-1) and Muscle Atrophy F-box protein (MAFBx). Moreover, an overexpression of both sarco/endoplasmic Ca²⁺-ATPase (SERCA1) and adenine nucleotide translocator (ANT1), both factors related to cellular energetic efficiency, was observed. Tumor burden also leads to a marked decreased in muscle ATP content. CONCLUSIONS: In addition to muscle proteolysis, other ATP-related pathways may have a key role in muscle wasting, both directly by increasing energetic inefficiency, and indirectly, by affecting the sarcoplasmic reticulum–mitochondrial assembly that is essential for muscle function and homeostasis. GENERAL SIGNIFICANCE: The present study reports profound morphological changes in cancer cachectic muscle, which are visualized mainly in alterations in sarcoplasmic reticulum and mitochondria. These alterations are linked to pathways that can account for energy inefficiency associated with cancer cachexia. |
| Author | Silva, Ana Paula García, Albert Sette, Angelica Sirisi, Sònia López-Soriano, Francisco J. Olivan, Mireia Fontes-Oliveira, Cibely Cristine Aylwin, Maria Paz Orpí, Marcel Busquets, Sílvia Toledo, Míriam Penna, Fabio Genovese, Maria Inês Argilés, Josep M. |
| Author_xml | – sequence: 1 givenname: Cibely Cristine surname: Fontes-Oliveira fullname: Fontes-Oliveira, Cibely Cristine organization: Cancer Research Group, Departament de Bioquímica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, Diagonal 645 08028-Barcelona, Spain – sequence: 2 givenname: Sílvia surname: Busquets fullname: Busquets, Sílvia email: silviabusquets@ub.edu organization: Cancer Research Group, Departament de Bioquímica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, Diagonal 645 08028-Barcelona, Spain – sequence: 3 givenname: Míriam surname: Toledo fullname: Toledo, Míriam organization: Cancer Research Group, Departament de Bioquímica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, Diagonal 645 08028-Barcelona, Spain – sequence: 4 givenname: Fabio surname: Penna fullname: Penna, Fabio organization: Dipartimento di Medicina e Oncologia Sperimentale, Università di Torino, Torino, Italy – sequence: 5 givenname: Maria Paz surname: Aylwin fullname: Aylwin, Maria Paz organization: Cancer Research Group, Departament de Bioquímica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, Diagonal 645 08028-Barcelona, Spain – sequence: 6 givenname: Sònia surname: Sirisi fullname: Sirisi, Sònia organization: Cancer Research Group, Departament de Bioquímica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, Diagonal 645 08028-Barcelona, Spain – sequence: 7 givenname: Ana Paula surname: Silva fullname: Silva, Ana Paula organization: Cancer Research Group, Departament de Bioquímica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, Diagonal 645 08028-Barcelona, Spain – sequence: 8 givenname: Marcel surname: Orpí fullname: Orpí, Marcel organization: Cancer Research Group, Departament de Bioquímica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, Diagonal 645 08028-Barcelona, Spain – sequence: 9 givenname: Albert surname: García fullname: García, Albert organization: Cancer Research Group, Departament de Bioquímica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, Diagonal 645 08028-Barcelona, Spain – sequence: 10 givenname: Angelica surname: Sette fullname: Sette, Angelica organization: Cancer Research Group, Departament de Bioquímica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, Diagonal 645 08028-Barcelona, Spain – sequence: 11 givenname: Maria Inês surname: Genovese fullname: Genovese, Maria Inês organization: Cancer Research Group, Departament de Bioquímica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, Diagonal 645 08028-Barcelona, Spain – sequence: 12 givenname: Mireia surname: Olivan fullname: Olivan, Mireia organization: Cancer Research Group, Departament de Bioquímica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, Diagonal 645 08028-Barcelona, Spain – sequence: 13 givenname: Francisco J. surname: López-Soriano fullname: López-Soriano, Francisco J. organization: Cancer Research Group, Departament de Bioquímica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, Diagonal 645 08028-Barcelona, Spain – sequence: 14 givenname: Josep M. surname: Argilés fullname: Argilés, Josep M. organization: Cancer Research Group, Departament de Bioquímica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, Diagonal 645 08028-Barcelona, Spain |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23200745$$D View this record in MEDLINE/PubMed |
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| Snippet | Cachexia is a wasting condition that manifests in several types of cancer, and the main characteristic is the profound loss of muscle mass.
The Yoshida AH-130... BACKGROUND: Cachexia is a wasting condition that manifests in several types of cancer, and the main characteristic is the profound loss of muscle mass.... Cachexia is a wasting condition that manifests in several types of cancer, and the main characteristic is the profound loss of muscle mass.BACKGROUNDCachexia... Cachexia is a wasting condition that manifests in several types of cancer, and the main characteristic is the profound loss of muscle mass.The Yoshida AH-130... |
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| SubjectTerms | Adenine Nucleotide Translocator 1 - genetics Adenine Nucleotide Translocator 1 - metabolism adenosine triphosphate Adenosine Triphosphate - deficiency Animals ANT1 apoptosis Apoptosis - genetics Ca2-transporting ATPase cachexia Cachexia - complications Cachexia - metabolism Cachexia - pathology Cancer cachexia Cell Nucleus - metabolism Cell Nucleus - ultrastructure energy efficiency Energy Metabolism - genetics F-box proteins Gene Expression homeostasis Male Mitochondri mitochondria Mitochondria - metabolism Mitochondria - ultrastructure Muscle Proteins - genetics Muscle Proteins - metabolism Muscle wasting Muscle, Skeletal - metabolism Muscle, Skeletal - pathology muscles muscular atrophy Muscular Atrophy - complications Muscular Atrophy - metabolism Muscular Atrophy - pathology Proteolysis quantitative polymerase chain reaction Rats Rats, Wistar Sarcoma, Yoshida - complications Sarcoma, Yoshida - metabolism Sarcoma, Yoshida - pathology Sarcoplasmic reticulum Sarcoplasmic Reticulum - metabolism Sarcoplasmic Reticulum - ultrastructure Sarcoplasmic Reticulum Calcium-Transporting ATPases - genetics Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism SERCA SKP Cullin F-Box Protein Ligases - genetics SKP Cullin F-Box Protein Ligases - metabolism transmission electron microscopy Tripartite Motif Proteins ubiquitin-protein ligase Ubiquitin-Protein Ligases - genetics Ubiquitin-Protein Ligases - metabolism Western blotting |
| Title | Mitochondrial and sarcoplasmic reticulum abnormalities in cancer cachexia: Altered energetic efficiency? |
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