ArticleCancer cell international2023
Targeting MYH9 represses USP14-mediated NAP1L1 deubiquitination and cell proliferation in glioma.
Article in Cancer cell international, 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, 18 citations in OpenAlex.
- A prognostic gene signature derived from aging-related genes predicts survival, immune landscape and therapy response in glioma.Molecular and clinical oncology · 2026Article
- USP14-mediated stabilization of ACTN1 maintains mesenchymal characteristics in glioblastoma.Communications biology · 2025Article
- ARHGAP4/MYH9/β-catenin/c-Jun positive feedback loop promotes colorectal cancer stemness.NPJ precision oncology · 2025Article
- Antibody MYH9 and Antibiotic Lidamycin Inhibit the Growth and Proliferation of Lung Cancer Cells and Induce Their Apoptosis.Molecular biotechnology · 2025Article
- Role of myosin heavy chain 9 in gastrointestinal tumorigenesis: A comprehensive review.World journal of gastrointestinal oncology · 2025Review
- MYH9 promotes malignant progression of glioma cells through regulating β-catenin stability via epithelial-mesenchymal transition signaling pathway.Scientific reports · 2025Article
- FATS inhibits the Wnt pathway and induces apoptosis through degradation of MYH9 and enhances sensitivity to paclitaxel in breast cancer.Cell death & disease · 2024Article
- A novel role for KIFC1-MYH9 interaction in triple-negative breast cancer aggressiveness and racial disparity.Cell communication and signaling : CCS · 2024Article
- Exploring the nexus between MYH9 and tumors: novel insights and new therapeutic opportunities.Frontiers in cell and developmental biology · 2024Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
Myosin heavy chain 9 (MYH9) plays an important role in a number of diseases. Nevertheless, the function of MYH9 in glioma is unclear. The present research aimed to investigate the role of MYH9 in glioma and determine whether MYH9 is involved in the temozolomide chemoresistance of glioma cells. Our results showed that MYH9 increased the proliferation and temozolomide resistance of glioma cells. The mechanistic experiments showed that the binding of MYH9 to NAP1L1, a potential promoter of tumor proliferation, inhibited the ubiquitination and degradation of NAP1L1 by recruiting USP14. Upregulation of NAP1L1 increased its binding with c-Myc and activated c-Myc, which induced the expression of CCND1/CDK4, promoting glioma cell temozolomide resistance and proliferation. Additionally, we found that MYH9 upregulation was strongly related to patient survival and is therefore a negative factor for patients with glioma. Altogether, our results show that MYH9 plays a role in glioma progression by regulating NAP1L1 deubiquitination. Thus, targeting MYH9 is a potential therapeutic strategy for the clinical treatment of glioma in the future.
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Registered trials
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