Abstract
Glioma is the most common and fatal primary brain tumor in humans. Myosin binding protein H (MYBPH), which was first identified as an important myofibrillar constituent of vertebrate skeletal and cardiac muscles, reduces cell motility and metastasis. However, its role in gliomas remains unclear. We evaluated the expression of MYBPH in glioma using Gene Expression Profiling Interactive Analysis (http://gepia.cancer-pku.cn/) and Chinese Glioma Genome Atlas (https://www.cgga.org.cn/). The results showed that MYBPH was highly expressed in glioma tissues. Moreover, MYBPH expression was significantly associated with high tumor aggressiveness and poor outcomes in glioma patients. Mechanistically, the results suggested that MYBPH might promote tumor progression by improving tumor invasion and migration. Our results establish MYBPH as an important prognostic biomarker that could be considered a potential epigenetic and immunotherapeutic target for treatment. We showed that MYBPH is a novel biomarker that is variably expressed in glioblastoma (GBM). The association of high MYBPH expression with poor prognosis in newly diagnosed GBM patients and increased expression in recurrent GBM is indicative of its role in tumor aggressiveness.
Highlights
Glioma is the most common primary malignant tumor of the central nervous s ystem[1]
Research suggests that myosin binding protein H (MYBPH) is a transcriptional target of thyroid transcription factor-1 (TTF-1), which reduces cell movement and metastasis by inhibiting Rho-associated protein kinase 1 (ROCK1)[11]
Immunohistochemical results showed that MYBPH was upregulated in clinical specimens from GBM patients and MYBPH expression was higher in tumor tissues than in the corresponding peritumor tissues and normal tissues (Fig. 2)
Summary
Glioma is the most common primary malignant tumor of the central nervous s ystem[1]. Cell motility is one of the most important aspects of tumor invasion and it is regulated by a variety of growth factor receptors that are imbalanced or amplified in G BM6. These receptors can be targeted with specific drugs, the effectiveness of drug treatment is weakened to a great extent by signal cascade redundancy in G BM7,8. Research suggests that MYBPH is a transcriptional target of thyroid transcription factor-1 (TTF-1), which reduces cell movement and metastasis by inhibiting Rho-associated protein kinase 1 (ROCK1)[11]. We explored the role of MYBPH in the biological behavior of a glioma cell line
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