ArticleCell death & disease2020
A Cdh1-FoxM1-Apc axis controls muscle development and regeneration.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Identification and validation of glucocorticoid receptor and programmed cell death-related genes in spinal cord injury using machine learning.Scientific reports · 2025Article
- Foxm1 promotes differentiation of neural progenitors in the zebrafish inner ear.Developmental biology · 2025Article
- ABL1-mediated phosphorylation promotes FOXM1-related tumorigenicity by Increasing FOXM1 stability.Cell death and differentiation · 2024Article
- GTSE1 promotes nasopharyngeal carcinoma proliferation and angiogenesis by upregulating STMN1.Cell division · 2024Article
- Network visualization of genes involved in skeletal muscle myogenesis in livestock animals.BMC genomics · 2024Article
- Transcriptome sequencing promotes insights on the molecular mechanism of SKP-SC-EVs mitigating denervation-induced muscle atrophy.Molecular biology reports · 2023Article
- FOXM1: Functional Roles of FOXM1 in Non-Malignant Diseases.Biomolecules · 2023Review
- Protective role of FBXL19 in Streptococcus pneumoniae-induced lung injury in pneumonia immature mice.Journal of cardiothoracic surgery · 2023Article
- Genome-wide analysis of a cellular exercise model based on electrical pulse stimulation.Scientific reports · 2022Article
- c-FLIP promotes drug resistance in non-small-cell lung cancer cells via upregulating FoxM1 expression.Acta pharmacologica Sinica · 2022Article
- Article
- An analysis of lncRNA-miRNA-mRNA networks to investigate the effects of HDAC4 inhibition on skeletal muscle atrophy caused by peripheral nerve injury.Annals of translational medicine · 2022Article
- In vivo cyclic induction of the FOXM1 transcription factor delays natural and progeroid aging phenotypes and extends healthspan.Nature aging · 2022Article
- USP39 facilitates breast cancer cell proliferation through stabilization of FOXM1.American journal of cancer research · 2022Article
- A Functional Network Model of the Metastasis Suppressor PEBP1/RKIP and Its Regulators in Breast Cancer Cells.Cancers · 2021Article
- FOXM1: A Multifunctional Oncoprotein and Emerging Therapeutic Target in Ovarian Cancer.Cancers · 2021Review
- Article
- Single-keratinocyte transcriptomic analyses identify different clonal types and proliferative potential mediated by FOXM1 in human epidermal stem cells.Nature communications · 2021Article
- GTSE1 promotes prostate cancer cell proliferation via the SP1/FOXM1 signaling pathway.Laboratory investigation; a journal of technical methods and pathology · 2021Article
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Forkhead box M1 (FoxM1) transcriptional factor has a principal role in regulating cell proliferation, self-renewal, and tumorigenesis. However, whether FoxM1 regulates endogenous muscle development and regeneration remains unclear. Here we found that loss of FoxM1 in muscle satellite cells (SCs) resulted in muscle atrophy and defective muscle regeneration. FoxM1 functioned as a direct transcription activator of adenomatous polyposis coli (Apc), preventing hyperactivation of wnt/β-catenin signaling during muscle regeneration. FoxM1 overexpression in SCs promoted myogenesis but impaired muscle regeneration as a result of spontaneous activation and exhaustion of SCs by transcriptional regulation of Cyclin B1 (Ccnb1). The E3 ubiquitin ligase Cdh1 (also termed Fzr1) was required for FoxM1 ubiquitylation and subsequent degradation. Loss of Cdh1 promoted quiescent SCs to enter into the cell cycle and the SC pool was depleted by serial muscle injuries. Haploinsufficiency of FoxM1 ameliorated muscle regeneration of Cdh1 knock-out mice. These data demonstrate that the Cdh1-FoxM1-Apc axis functions as a key regulator of muscle development and regeneration.
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Registered trials
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.