ArticleBritish journal of cancer2005
NF-kappaB mediates proteolysis-inducing factor induced protein degradation and expression of the ubiquitin-proteasome system in skeletal muscle.
Article in British journal of cancer, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 129 citations in OpenAlex.
- Seric Molecular Markers Correlated with Stroke Rehabilitation Outcomes: A Narrative Review.Life (Basel, Switzerland) · 2026Review
- Muscle Insulin Resistance Elicits Muscle Atrophy in Obesity.Current obesity reports · 2025Review
- Signaling networks governing skeletal muscle growth, atrophy, and cachexiaSkeletal muscle · 2025Review
- Targeting ROS in cancer: rationale and strategies.Nature reviews. Drug discovery · 2024Review
- Why do patients with cancer die?Nature reviews. Cancer · 2024Review
- Increased Expression of Proinflammatory Genes in Peripheral Blood Cells Is Associated with Cardiac Cachexia in Patients with Heart Failure with Reduced Ejection Fraction.Journal of clinical medicine · 2024Article
- Review
- Towards Drug Repurposing in Cancer Cachexia: Potential Targets and Candidates.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Pancreatic cancer cachexia: three dimensions of a complex syndrome.British journal of cancer · 2021Review
- NexrutinePhysiological reports · 2019Article
- Updates on the pathogenesis of advanced lung cancer-induced cachexia.Thoracic cancer · 2019Review
- Chemotherapy-induced muscle wasting: association with NF-κB and cancer cachexia.European journal of translational myology · 2018Article
- The role of sex steroid hormones in the pathophysiology and treatment of sarcopenia.Osteoporosis and sarcopenia · 2016Review
- Molecular pathways leading to loss of skeletal muscle mass in cancer cachexia--can findings from animal models be translated to humans?BMC cancer · 2016Review
- The Janus-Faced Role of Antioxidants in Cancer Cachexia: New Insights on the Established Concepts.Oxidative medicine and cellular longevity · 2016Review
- Skeletal muscle atrophy: disease-induced mechanisms may mask disuse atrophy.Journal of muscle research and cell motility · 2015Review
- Tumor macroenvironment and metabolism.Seminars in oncology · 2014Review
- Pancreatic cancer cachexia: a review of mechanisms and therapeutics.Frontiers in physiology · 2014Review
- Oxidative stress, NF-κB and the ubiquitin proteasomal pathway in the pathology of calpainopathy.Neurochemical research · 2013Article
- Mechanisms underlying the anti-wasting effect of L-carnitine supplementation under pathologic conditions: evidence from experimental and clinical studies.European journal of nutrition · 2013Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Loss of skeletal muscle in cancer cachexia has a negative effect on both morbidity and mortality. The role of nuclear factor-kappaB (NF-kappaB) in regulating muscle protein degradation and expression of the ubiquitin-proteasome proteolytic pathway in response to a tumour cachectic factor, proteolysis-inducing factor (PIF), has been studied by creating stable, transdominant-negative, muscle cell lines. Murine C(2)C(12) myoblasts were transfected with plasmids with a CMV promoter that had mutations at the serine phosphorylation sites required for degradation of I-kappaBalpha, an NF-kappaB inhibitory protein, and allowed to differentiate into myotubes. Proteolysis-inducing factor induced degradation of I-kappaBalpha, nuclear accumulation of NF-kappaB and an increase in luciferase reporter gene activity in myotubes containing wild-type, but not mutant, I-kappaBalpha proteins. Proteolysis-inducing factor also induced total protein degradation and loss of the myofibrillar protein myosin in myotubes containing wild-type, but not mutant, plasmids at the same concentrations as those causing activation of NF-kappaB. Proteolysis-inducing factor also induced increased expression of the ubiquitin-proteasome pathway, as determined by 'chymotrypsin-like' enzyme activity, the predominant proteolytic activity of the beta-subunits of the proteasome, protein expression of 20S alpha-subunits and the 19S subunits MSS1 and p42, as well as the ubiquitin conjugating enzyme, E2(14k), in cells containing wild-type, but not mutant, I-kappaBalpha. The ability of mutant I-kappaBalpha to inhibit PIF-induced protein degradation, as well as expression of the ubiquitin-proteasome pathway, confirms that both of these responses depend on initiation of transcription by NF-kappaB.
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