ArticleAmerican journal of physiology. Cell physiology2021
Breast cancer-associated skeletal muscle mitochondrial dysfunction and lipid accumulation is reversed by PPARG.
Article in American journal of physiology. Cell physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 56 citations in OpenAlex.
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Trial
- Skeletal muscle-specific myostatin overexpression promotes muscle oxidative capacity and fatigue resistance in transgenic mice.Experimental physiology · 2026Article
- A cohort study investigating differences in skeletal muscle mitochondrial function between prostate cancer patients and healthy controls.BMC cancer · 2026Article
- Single-fiber morphometry and spatial transcriptomics reveal selective oxidative muscle fiber atrophy in non-metastatic breast cancer.medRxiv : the preprint server for health sciences · 2026Article
- Characterization of body composition dynamics throughout treatment in patients with early-stage breast cancer.NPJ breast cancer · 2026Article
- Metabolic and skeletal muscle dysfunctions correlate with fatigue behavior in an animal model of multiple sclerosis.Frontiers in physiology · 2026Article
- Early Markers of Cardiac and Skeletal Muscle Metabolic Derangement in the Apc(min/+) Male Mouse.Cancer reports (Hoboken, N.J.) · 2025Article
- Transient increase in mitochondrial respiration in blood cells from breast cancer patients following chemo- and radiotherapy.Clinical and experimental medicine · 2025Article
- Exploring the mechanism of rosmarinic acid in the treatment of lung adenocarcinoma based on bioinformatics methods and experimental validation.Discover oncology · 2025Article
- Mechanisms, assessment, and exercise interventions for skeletal muscle dysfunction post-chemotherapy in breast cancer: from inflammation factors to clinical practice.Frontiers in oncology · 2025Review
- The role of PPARγ in cancer cachexia: friend or foe?Frontiers in endocrinology · 2025Review
- Thymidine exerts anti-doxorubicin-induced cardiomyopathy effect through the regulation of the PPAR signaling pathways and ferroptosis pathways.Frontiers in pharmacology · 2025Article
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- Restoring Skeletal Muscle Health through Exercise in Breast Cancer Patients and after Receiving Chemotherapy.International journal of molecular sciences · 2024Review
- The cooperative regulatory effect of the miRNA-130 family on milk fat metabolism in dairy cows.Animal bioscience · 2024Article
- Myogenic microRNAs as Therapeutic Targets for Skeletal Muscle Mass Wasting in Breast Cancer Models.International journal of molecular sciences · 2024Review
- Preclinical Multi-Omic Assessment of Pioglitazone in Skeletal Muscles of Mice Implanted with Human HER2/neu Overexpressing Breast Cancer Xenografts.bioRxiv : the preprint server for biology · 2024Article
- Tumor-associated macrophage subtypes on cancer immunity along with prognostic analysis and SPP1-mediated interactions between tumor cells and macrophages.PLoS genetics · 2024Article
- A pilot study of mitochondrial response to an in vivo prosthetic joint Staphylococcus aureus infection model.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2024Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The peroxisome proliferator-activated receptors (PPARs) have been previously implicated in the pathophysiology of skeletal muscle dysfunction in women with breast cancer (BC) and animal models of BC. This study investigated alterations induced in skeletal muscle by BC-derived factors in an in vitro conditioned media (CM) system and tested the hypothesis that BC cells secrete a factor that represses PPAR-γ (PPARG) expression and its transcriptional activity, leading to downregulation of PPARG target genes involved in mitochondrial function and other metabolic pathways. We found that BC-derived factors repress PPAR-mediated transcriptional activity without altering protein expression of PPARG. Furthermore, we show that BC-derived factors induce significant alterations in skeletal muscle mitochondrial function and lipid accumulation, which are rescued with exogenous expression of PPARG. The PPARG agonist drug rosiglitazone was able to rescue BC-induced lipid accumulation but did not rescue effects of BC-derived factors on PPAR-mediated transcription or mitochondrial function. These data suggest that BC-derived factors alter lipid accumulation and mitochondrial function via different mechanisms that are both related to PPARG signaling, with mitochondrial dysfunction likely being altered via repression of PPAR-mediated transcription, and lipid accumulation being altered via transcription-independent functions of PPARG.
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