ArticleThe Biochemical journal2012
Myostatin is a novel tumoral factor that induces cancer cachexia.
Article in The Biochemical journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 38 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
38 citing papers in PubMed, 96 citations in OpenAlex.
- Oleanolic acid alleviates obesity-induced skeletal muscle atrophy via the PI3K/Akt signaling pathway.FEBS open bio · 2024Article
- Cancer-triggered systemic disease and therapeutic targets.Holistic integrative oncology · 2024Article
- Targeting Epigenetic Regulators with HDAC and BET Inhibitors to Modulate Muscle Wasting.International journal of molecular sciences · 2023Review
- Activin A promotes cell proliferation, invasion and migration and predicts poor prognosis in patients with colorectal cancer.Oncology reports · 2022Article
- Hormonally Regulated Myogenic miR-486 Influences Sex-specific Differences in Cancer-induced Skeletal Muscle Defects.Endocrinology · 2021Article
- Article
- A review of the current concerns about misconduct in medical sciences publications and the consequences.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2020Review
- Molecular therapeutic strategies targeting pancreatic cancer induced cachexia.World journal of gastrointestinal surgery · 2018Review
- Myostatin knockout induces apoptosis in human cervical cancer cells via elevated reactive oxygen species generation.Redox biology · 2018Article
- Petri net-based prediction of therapeutic targets that recover abnormally phosphorylated proteins in muscle atrophy.BMC systems biology · 2018Article
- Acylated and unacylated ghrelin inhibit atrophy in myotubes co-cultured with colon carcinoma cells.Oncotarget · 2017Article
- Molecular mechanism of sarcopenia and cachexia: recent research advances.Pflugers Archiv : European journal of physiology · 2017Review
- Activin A induces skeletal muscle catabolism via p38β mitogen-activated protein kinase.Journal of cachexia, sarcopenia and muscle · 2017Article
- Redox regulation of autophagy in skeletal muscle.Free radical biology & medicine · 2016Review
- Pay attention to cardiac remodeling in cancer cachexia.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2016Review
- The emerging role of skeletal muscle oxidative metabolism as a biological target and cellular regulator of cancer-induced muscle wasting.Seminars in cell & developmental biology · 2016Review
- Cardiac cachexia: hic et nunc.Journal of cachexia, sarcopenia and muscle · 2016Review
- Cancer cachexia-when proteasomal inhibition is not enough.Journal of cachexia, sarcopenia and muscle · 2016Article
- Citrus unshiu peel extract alleviates cancer-induced weight loss in mice bearing CT-26 adenocarcinoma.Scientific reports · 2016Article
- Pancreatic cancer cell-derived IGFBP-3 contributes to muscle wasting.Journal of experimental & clinical cancer research : CR · 2016Article
Corrections and comments
- Retraction · 2016-04-15Falsification/Fabrication of Data · Investigation by Company/Institution · Misconduct by Author ·
- Erratum issued
- Retracted
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Humoral and tumoral factors collectively promote cancer-induced skeletal muscle wasting by increasing protein degradation. Although several humoral proteins, namely TNFα (tumour necrosis factor α) and IL (interleukin)-6, have been shown to induce skeletal muscle wasting, there is a lack of information regarding the tumoral factors that contribute to the atrophy of muscle during cancer cachexia. Therefore, in the present study, we have characterized the secretome of C26 colon cancer cells to identify the tumoral factors involved in cancer-induced skeletal muscle wasting. In the present study, we show that myostatin, a procachectic TGFβ (transforming growth factor β) superfamily member, is abundantly secreted by C26 cells. Consistent with myostatin signalling during cachexia, treating differentiated C2C12 myotubes with C26 CM (conditioned medium) resulted in myotubular atrophy due to the up-regulation of muscle-specific E3 ligases, atrogin-1 and MuRF1 (muscle RING-finger protein 1), and enhanced activity of the ubiquitin-proteasome pathway. Furthermore, the C26 CM also activated ActRIIB (activin receptor type II B)/Smad and NF-κB (nuclear factor κB) signalling, and reduced the activity of the IGF-I (insulin-like growth factor 1)/PI3K (phosphoinositide 3-kinase)/Akt pathway, three salient molecular features of myostatin action in skeletal muscles. Antagonists to myostatin prevented C26 CM-induced wasting in muscle cell cultures, further confirming that tumoral myostatin may be a key contributor in the pathogenesis of cancer cachexia. Finally, we show that treatment with C26 CM induced the autophagy-lysosome pathway and reduced the number of mitochondria in myotubes. These two previously unreported observations were recapitulated in skeletal muscles collected from C26 tumour-bearing mice.
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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.