Abstract
BackgroundCurrent treatment options for glioma are limited, and the prognosis of patients with glioma is poor as the available drugs show low therapeutic efficacy. Furthermore, the molecular mechanisms associated with glioma remain poorly understood. METTL1 mainly catalyzes the formation of N(7)-methylguanine at position 46 of the transfer RNA sequence, thereby regulating the translation process. However, the role of METTL1 in glioma has not been studied to date. The purpose of this study was to analyze the expression and prognosis of METTL1 in glioma, and to explore the potential analysis mechanism.MethodsData from five publicly available databases were used to analyze METTL1 expression across different tumor types and its differential expression between carcinoma and adjacent normal tissues. The expression of METTL1 in glioma was further validated using real-time polymerase chain reaction and immunohistochemistry. Meanwhile, siRNA was used to knockdown METTL1 in U87 glioma cells, and the resultant effect on glioma proliferation was verified using the Cell Counting Kit 8 (CCK8) assay. Furthermore, a nomogram was constructed to predict the association between METTL1 expression and the survival rate of patients with glioma.ResultsMETTL1 expression increased with increasing glioma grades and was significantly higher in glioma than in adjacent noncancerous tissues. In addition, high expression of METTL1 promoted cell proliferation. Moreover, METTL1 expression was associated with common clinical risk factors and was significantly associated with the prognosis and survival of patients with glioma. Univariate and multivariate Cox regression analyses revealed that METTL1 expression may be used as an independent prognostic risk factor for glioma. Furthermore, results of functional enrichment and pathway analyses indicate that the mechanism of METTL1 in glioma is potentially related to the MAPK signaling pathway.ConclusionsHigh METTL1 expression is significantly associated with poor prognosis of patients with glioma and may represent a valuable independent risk factor. In addition, high expression of METTL1 promotes glioma proliferation and may regulate mitogen-activated protein kinase (MAPK) signaling pathway. Thus, METTL1 may be a potential biomarker for glioma. Further investigations are warranted to explore its clinical use.
Highlights
Current treatment options for glioma are limited, and the prognosis of patients with glioma is poor as the available drugs show low therapeutic efficacy
Methyltransferase-like 1 (METTL1) expression across cancer and normal tissues The expression of METTL1 was found to be lower in normal human blood and brain tissues than in other normal tissues (Fig. 2a), whereas it was similar across various cancer cell lines (Fig. 2b)
METTL1 expression was found to be significantly higher in bladder urothelial carcinoma, breast invasive carcinoma, cholangiocarcinoma, colon adenocarcinoma, esophageal carcinoma, GBM, head and neck squamous cell carcinoma, kidney renal clear cell carcinoma (KIRC), liver hepatocellular carcinoma (LIHC), lung adenocarcinoma, lung squamous cell carcinoma, prostate adenocarcinoma, rectum adenocarcinoma, stomach adenocarcinoma, thyroid carcinoma, thymoma, and uterine corpus endometrial carcinoma tissues than in the corresponding normal tissues (Fig. 2c)
Summary
Current treatment options for glioma are limited, and the prognosis of patients with glioma is poor as the available drugs show low therapeutic efficacy. The purpose of this study was to analyze the expression and prognosis of METTL1 in glioma, and to explore the potential analysis mechanism. Overexpression of METTL1 enhanced the cytotoxic effect of cisplatin on cisplatin-resistant colon cancer cells by mir149-3p action via the S100A4/p53 signaling pathway [6], and induced the expression of NANOG and Kruppel Like Factor 4 (KLF4) [7], two phosphatase and tensin homolog (PTEN-regulated molecules [8], and promoted carcinogenicity in hepatocellular carcinoma (HCC) via the PTEN/AKT axis [9]. We speculated that in addition to its role in tumors, METTL1 expression may be increased in gliomas and may promote the progression of gliomas, thereby affecting the prognosis of patients
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