ArticleCell cycle (Georgetown, Tex.)2023
USP38 inhibits colorectal cancer cell proliferation and migration via downregulating HMX3 ubiquitylation.
Article in Cell cycle (Georgetown, Tex.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Quantification of DNA Methylation for Diagnosis and Monitoring of Hepatocellular Carcinoma.Journal of the American College of Surgeons · 2026Article
- The role of ubiquitination in the pathogenesis of atrial fibrillation: mechanisms and therapeutic implications.Frontiers in pharmacology · 2026Review
- ILF3 Regulates Cell Proliferation and Metastasis by Competitively Antagonizing the Interaction Between HMGCL and USP38 in Hepatocellular Carcinoma.Human mutation · 2026Article
- Review
- Ubiquitin-specific proteases as key regulators in the malignant progression and therapy resistance of colorectal cancer: current insights and future perspectives.Discover oncology · 2025Review
- USP38: an important regulatory factor in tumor malignant progression.Frontiers in immunology · 2025Review
- Crosstalk Between the Nervous System and Colorectal Cancer.Neuroscience bulletin · 2025Review
- Comprehensive analysis of the role of ubiquitin-specific peptidases in colorectal cancer: A systematic review.World journal of gastrointestinal oncology · 2024Article
- Ubiquitin specific protease 38 aggravates pathological cardiac remodeling by stabilizing phospho-TBK1.International journal of biological sciences · 2024Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence has shown that H6 Family Homeobox 3 (HMX3) plays a crucial role in nervous system regulation. However, the regulatory mechanism of HMX3 in colorectal cancer (CRC) has seldom been studied. Herein, HMX3 was significantly downregulated in CRC, as demonstrated by qRT-PCR and WB analysis on clinical samples and a panel of cell lines. Besides, it was found that the expression of HMX3 was negatively correlated with survival of CRC patients. The functional analyses (EdU staining, CCK-8, colony formation, Transwell, and wound scratch assays) showed that CRC cell proliferation, migration, and invasion were significantly suppressed by HMX3 overexpression, while enhanced by HMX3 knockdown. Moreover,
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Registered trials
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