Twist1 Activation in Muscle Progenitor Cells Causes Muscle Loss Akin to Cancer Cachexia
Open accessAbstract
Cancer cachexia is characterized by extreme skeletal muscle loss that results in high morbidity and mortality. The incidence of cachexia varies among tumor types, being lowest in sarcomas, whereas 90% of pancreatic ductal adenocarcinoma (PDAC) patients experience severe weight loss. How these tumors trigger muscle depletion is still unfolding. Serendipitously, we found that overexpression of Twist1 in mouse muscle progenitor cells, either constitutively during development or inducibly in adult animals, caused severe muscle atrophy with features reminiscent of cachexia. Using several genetic mouse models of PDAC, we detected a marked increase in Twist1 expression in muscle undergoing cachexia. In cancer patients, elevated levels of Twist1 are associated with greater degrees of muscle wasting. Finally, both genetic and pharmacological inactivation of Twist1 in muscle progenitor cells afforded substantial protection against cancer-mediated cachexia, which translated into meaningful survival benefits, implicating Twist1 as a possible target for attenuating muscle cachexia in cancer patients.
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Induction of myostatin in satellite cells and its secretion induces secondary Smad2/3-dependent expression of Twist in adult myofibers that by synergizing with Smads activates atrophy program.
“The induction of myostatin in satellite cells and its secretion induces a secondary Smad2/3-dependent expression of Twist is adult myofibers that by synergizing with the Smads activates the atrophy program86 (Fig. 5).”
From Mechanisms of muscle atrophy and hypertrophy: implications in health and disease (2021) · cites this paper as [86]
Activation of TGFβ signaling in muscle stem cells upregulates Twist-1, which enhances myostatin expression.
“Consistently, the activation of TGFβ signaling in muscle stem cells upregulates the Twist-1 transcription factor, which enhances myostatin expression.”
From Mechanisms of muscle atrophy and hypertrophy: implications in health and disease (2021) · cites this paper as [86]
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Razzaque, M. S., & Atfi, A. (2020) · Frontiers in Physiology · doi:10.3389/fphys.2020.00662 · Cited by 7 · see citing works
Self-citationThe mechanism by which noncoding RNAs regulate muscle wasting in cancer cachexia
Zhou, X., Hu, S., Zhang, Y., Du, G., & Li, Y. (2021) · Precision Clinical Medicine · doi:10.1093/pcmedi/pbab008 · Cited by 7 · see citing works
Pancreatic cancer cachexia: A systemic consequence of multi-organ interactions
Xiao, A., Feng, Y., Yin, B., Zhang, J., Cao, Z., Liu, X., Liang, Y., & Wu, W. (2025) · hLife · doi:10.1016/j.hlife.2025.05.002 · Cited by 6 · see citing works
Temporal dynamics of gene and protein signatures following volumetric muscle loss
Jain, I., Oropeza, B. P., Hu, C., Chiang, G., Aravindan, S., Reyes, R., Li, D. Y., Cheng, P. P., & Huang, N. F. (2025) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2025.1606609 · Cited by 4 · see citing works
NF-kB Signaling in the Macroenvironment of Cancer Cachexia
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The myoblast methylome: multiple types of associations with chromatin and transcription
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Advancing cancer cachexia diagnosis with -omics technology and exercise as molecular medicine
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From rock ‘n’ roll to heavy metal
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MyoRep: A Novel Reporter System to Detect Early Muscle Atrophy In Vitro and In Vivo
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Twist1 overexpression models an aggressive subtype of pancreatic ductal adenocarcinoma in vivo
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- Authors
- Parajuli, P., Kumar, S., Loumaye, A., Singh, P., Eragamreddy, S., Nguyen, T. L., Ozkan, S., Razzaque, M. S., Prunier, C., Thissen, J.-P., & Atfi, A.
- Affiliations
- University of Mississippi Medical Center (US)
- UCLouvain (BE)
- Harvard University (US)
- Inserm (FR)
- Corresponding author
- Atfi, Azeddine
- ORCID
- Venue
- Developmental Cell
- Publisher
- Elsevier BV
- Published
- 2018-06
- Volume
- 45
- Issue
- 6
- Pages
- 712-725.e6
- ISSN
- 1534-5807 (ISSN-L)
- PMC
- PMC6054474
- OpenAlex
- W2808843677
- Cited by
- 58
- References
- 44
- Citations by year
- 2026: 3 · 2025: 5 · 2024: 8 · 2023: 7 · 2022: 7 · 2021: 8 · 2020: 13 · 2019: 5 · 2018: 2
- FWCI
- 2.49
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 382 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Developmental Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion)
- Digital Access to Libraries (Université catholique de Louvain (UCL), l'Université de Namur (UNamur) and the Université Saint-Louis (USL-B)) (submittedVersion, other-oa)
- Funders
- Ministry of Public Health
- Fondation Saint Luc
- National Institutes of Health (R01-AR059070, R01-CA210911)
- U.S. Department of Defense (PR152164, PR162051)
- Australian Research Council
- Association pour la Recherche sur le Cancer
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Physiology › Nutrition and Health in Aging
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Sarcoma Diagnosis and Treatment
- Keywords
- TWIST1, cancer cachexia, muscle atrophy, muscle progenitor cells, pancreatic ductal adenocarcinoma, skeletal muscle atrophy, therapeutic target
- MeSH terms
- Animals, Cachexia, Humans, Lung Neoplasms, Male, Mice, Inbred C57BL, Muscular Atrophy, Nuclear Proteins, Stem Cells, Colorectal Neoplasms, Signal Transduction, Muscle, Skeletal, Muscle Cells, Myoblasts, Cell Line, Tumor, Mice, Twist-Related Protein 1, HEK293 Cells
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