ArticleFrontiers in physiology2014
Mitochondria dysfunction in lung cancer-induced muscle wasting in C2C12 myotubes.
Article in Frontiers in physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Bibliometric and visualization analyses of cancer-related fatigue research published worldwide from 2001 to 2023.Frontiers in oncology · 2024Pooled it
- The Secretome of a Cachexia-Inducing Lung Tumor Impairs Mitochondrial Function and Skeletal Muscle Differentiation.Cancers · 2026Article
- Cancer cachexia: A tumor-driven disorder of whole-body homeostasis.Cancer cell · 2026Review
- Vitamin B1 Involved inInternational journal of molecular sciences · 2025Article
- Physical Activity, Exerkines, and Their Role in Cancer Cachexia.International journal of molecular sciences · 2025Review
- Restoring Skeletal Muscle Health through Exercise in Breast Cancer Patients and after Receiving Chemotherapy.International journal of molecular sciences · 2024Review
- Mitochondria transcription and cancer.Cell death discovery · 2024Review
- Immunoregulation in cancer-associated cachexia.Journal of advanced research · 2024Review
- Cholic and deoxycholic acids induce mitochondrial dysfunction, impaired biogenesis and autophagic flux in skeletal muscle cells.Biological research · 2023Article
- Article
- Chicken or Egg? Mitochondrial Phospholipids and Oxidative Stress in Disuse-Induced Skeletal Muscle Atrophy.Antioxidants & redox signaling · 2023Review
- Article
- The NLRP3 inflammasome contributes to inflammation-induced morphological and metabolic alterations in skeletal muscle.Journal of cachexia, sarcopenia and muscle · 2022Article
- The Role of Skeletal Muscle Mitochondria in Colorectal Cancer Related Cachexia: Friends or Foes?International journal of molecular sciences · 2022Review
- Bile Acids Induce Alterations in Mitochondrial Function in Skeletal Muscle Fibers.Antioxidants (Basel, Switzerland) · 2022Article
- Review
- Growth hormone secretagogue receptor-1a mediates ghrelin's effects on attenuating tumour-induced loss of muscle strength but not muscle mass.Journal of cachexia, sarcopenia and muscle · 2021Article
- Metabolic Remodeling in Skeletal Muscle Atrophy as a Therapeutic Target.Metabolites · 2021Review
- Pharmacological or genetic inhibition of iNOS prevents cachexia-mediated muscle wasting and its associated metabolism defects.EMBO molecular medicine · 2021Article
- Mitochondrial dynamics and quality control are altered in a hepatic cell culture model of cancer cachexia.Molecular and cellular biochemistry · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
aimsCancer cachexia is a syndrome which results in severe loss of muscle mass and marked fatigue. Conditioned media from cachexia-inducing cancer cells triggers metabolic dysfunction in skeletal muscle, including decreased mitochondrial respiration, which may contribute to fatigue. We hypothesized that Lewis lung carcinoma conditioned medium (LCM) would impair the mitochondrial electron transport chain (ETC) and increase production of reactive oxygen species, ultimately leading to decreased mitochondrial respiration. We incubated C2C12 myotubes with LCM for 30 min, 2, 4, 24 or 48 h. We measured protein content by western blot; oxidant production by 2',7'-dichlorofluorescin diacetate (DCF), 4-amino-5-methylamino-2',7'-difluorofluorescein diacetate (DAF), and MitoSox; cytochrome c oxidase activity by oxidation of cytochrome c substrate; and oxygen consumption rate (OCR) of intact myotubes by Seahorse XF Analyzer.
resultsLCM treatment for 2 or 24 h decreased basal OCR and ATP-related OCR, but did not alter the content of mitochondrial complexes I, III, IV and V. LCM treatment caused a transient rise in reactive oxygen species (ROS). In particular, mitochondrial superoxide (MitoSOX) was elevated at 2 h. 4-Hydroxynonenal, a marker of oxidative stress, was elevated in both cytosolic and mitochondrial fractions of cell lysates after LCM treatment.
conclusionThese data show that lung cancer-conditioned media alters electron flow in the ETC and increases mitochondrial ROS production, both of which may ultimately impair aerobic metabolism and decrease muscle endurance.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.