ArticleCell death & disease2021
An integrative transcriptome study reveals Ddit4/Redd1 as a key regulator of cancer cachexia in rodent models.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- C26 and CT26 colorectal cancer models exhibit divergent cachexia phenotypes, intramuscular inflammation, and protein turnover signaling.bioRxiv : the preprint server for biology · 2026Article
- Macrophage-Myocyte Cross Talk Induces M1 Polarization and Inflammatory Cytokine Production During Cancer Cachexia.Mediators of inflammation · 2026Article
- Fiber-type vulnerability and proteostasis reprogramming in skeletal muscle during pancreatic cancer cachexia.bioRxiv : the preprint server for biology · 2025Article
- Cachexia-induced reprogramming of visceral organ metabolism by human pancreatic cancer xenografts.International journal of cancer · 2025Article
- p38α MAPK Regulation of Energy Metabolism in Skeletal Muscle Offers a Therapeutic Path for Type 2 Diabetes.Cells · 2025Review
- Transcriptional analysis of cancer cachexia: conserved and unique features across preclinical models and biological sex.American journal of physiology. Cell physiology · 2024Article
- Unlocking Prognostic Genes and Multi-Targeted Therapeutic Bioactives from Herbal Medicines to Combat Cancer-Associated Cachexia: A Transcriptomics and Network Pharmacology Approach.International journal of molecular sciences · 2023Article
- Females display relatively preserved muscle quality compared with males during the onset and early stages of C26-induced cancer cachexia.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Article
- The time-course of cancer cachexia onset reveals biphasic transcriptional disruptions in female skeletal muscle distinct from males.BMC genomics · 2023Article
- Review
- Nutritional Sensor REDD1 in Cancer and Inflammation: Friend or Foe?International journal of molecular sciences · 2022Review
- The myokine Fibcd1 is an endogenous determinant of myofiber size and mitigates cancer-induced myofiber atrophy.Nature communications · 2022Article
- Tumor cell anabolism and host tissue catabolism-energetic inefficiency during cancer cachexia.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- TXNIP inhibits the progression of osteosarcoma through DDIT4-mediated mTORC1 suppression.American journal of cancer research · 2022Article
- Aberrant mitochondrial homeostasis at the crossroad of musculoskeletal ageing and non-small cell lung cancer.PloS one · 2022Article
- Aging Aggravates Cachexia in Tumor-Bearing Mice.Cancers · 2021Article
- REDD1 deletion attenuates cancer cachexia in mice.Journal of applied physiology (Bethesda, Md. : 1985) · 2021Article
- Low-Dose Metformin as a Monotherapy Does Not Reduce Non-Small-Cell Lung Cancer Tumor Burden in Mice.Biomedicines · 2021Article
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Cancer cachexia is a multifactorial metabolic syndrome that causes up to 20% of cancer-related deaths. Muscle atrophy, the hallmark of cancer cachexia, strongly impairs the quality of life of cancer patients; however, the underlying pathological process is still poorly understood. Investigation of the disease pathogenesis largely relies on cachectic mouse models. In our study, the transcriptome of the cachectic gastrocnemius muscle in the C26 xenograft model was integrated and compared with that of 5 more different datasets. The bioinformatic analysis revealed pivotal gene ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways of the disease, and the key genes were validated. Construction of the protein-protein interaction network and the comparison of pathways enriched in cancer cachexia with 5 other muscle atrophy models revealed Ddit4 (DNA damage-inducible transcript 4), as a key protein in cancer cachexia. The higher expression of Ddit4 in cachectic muscle was further validated in animal models and cachectic cancer patients. Further study revealed that p38 induced the expression of Ddit4, which in turn inhibited the mTOR pathway in atrophic cells.
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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.