Abstract
Recent studies have identified pleiotropic roles of methyltransferase-like 3 (METTL3) in tumor progression. However, the roles of METTL3 in esophageal squamous cell carcinoma (ESCC) are still unclear. Here, we investigated the function and mechanism of METTL3 in ESCC tumorigenesis. We reported that higher METTL3 expression was found in ESCC tissues and was markedly associated with depth of invasion and poor prognosis. Loss- and gain-of function studies showed that METTL3 promoted the migration and invasion of ESCC cells in vitro. Integrated methylated RNA immunoprecipitation sequencing (MeRIP-Seq) and RNA sequencing (RNA-Seq) analysis first demonstrated that glutaminase 2 (GLS2) was regulated by METTL3 via m6A modification. Our findings identified METTL3/GLS2 signaling as a potential therapeutic target in antimetastatic strategies against ESCC.
Highlights
Esophageal cancer is one of the most common malignant tumors worldwide, and it is the third most common cancer in China [1, 2]
Strong methyltransferase-like 3 (METTL3) staining was observed in esophageal squamous cell carcinoma (ESCC) tumor tissues
The IHC results showed that METTL3 expression was significantly higher in 71.7% (38/53) of the ESCC tissues than in the adjacent normal tissues (Figure 1C)
Summary
Esophageal cancer is one of the most common malignant tumors worldwide, and it is the third most common cancer in China [1, 2]. The 5-year relative survival rate for esophageal cancer is 20%, (localized 47%, regional 25%, distant 5%) [1]. Metastasis is a major cause of death in esophageal cancer patients. Esophageal squamous cell carcinoma (ESCC) is the major histological subtype of esophageal cancer in China [3]. Metastasis is found in over 60% of newly diagnosed cases, which is one of the principal reasons why the overall 5-year survival rate of esophageal cancer is
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