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Updated: Jul 15, 2025
In Vitro Ubiquitination and Deubiquitination Assays of Nucleosomal Histones
Published on: July 25, 2019
Targeting MYH9 represses USP14-mediated NAP1L1 deubiquitination and cell proliferation in glioma
Zigui Chen1,2, Xin Yan3, Changfeng Miao4
1Cancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, 13 Shiliugang ST, Guangzhou, 510315, China.
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.
Insights
Myosin heavy chain 9 (MYH9) promotes glioma cell proliferation and temozolomide resistance by stabilizing NAP1L1. Targeting MYH9 may offer a new therapeutic strategy for glioma patients.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Myosin heavy chain 9 (MYH9) is implicated in various diseases, but its role in glioma remains largely unknown.
- Understanding MYH9's function is crucial for developing targeted glioma therapies.
Purpose of the Study:
- To investigate the role of MYH9 in glioma progression.
- To determine if MYH9 influences temozolomide chemoresistance in glioma cells.
Main Methods:
- Investigated MYH9's effect on glioma cell proliferation and temozolomide resistance.
- Conducted mechanistic studies involving MYH9, NAP1L1, USP14, c-Myc, CCND1, and CDK4.
- Analyzed the correlation between MYH9 expression and patient survival.
Main Results:
- MYH9 significantly increased glioma cell proliferation and temozolomide resistance.
- MYH9 inhibited NAP1L1 ubiquitination and degradation by recruiting USP14, leading to NAP1L1 upregulation.
- Upregulated NAP1L1 activated c-Myc, inducing CCND1/CDK4 expression and promoting proliferation and chemoresistance.
- MYH9 upregulation correlated with poor patient survival in glioma.
Conclusions:
- MYH9 drives glioma progression and temozolomide resistance by regulating NAP1L1 deubiquitination.
- MYH9 represents a potential therapeutic target for improving glioma treatment outcomes.
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