Silencing of methyltransferase-like 3 inhibits oesophageal squamous cell carcinoma.

Methyltransferase-like 3 (METTL3) is a methyltransferase responsible for N6-methyladenosine mRNA modifications, which has been demonstrated to serve oncogenic roles in various types of cancer; however, the exact function of METTL3 in oesophageal squamous cell carcinoma (ESCC) has not been determined. The present study aimed to explore the regulatory role of METTL3 in ESCC. In the present study, reverse transcription-quantitative PCR and western blotting were used to examine mRNA and protein expression, CCK-8 assays and flow cytometry were used to determine cellular viability and apoptosis, and wound healing and Transwell assays were conducted to study cellular migration and invasion. The expression levels of METTL3 were significantly higher in ESCC tissues and cell lines compared with adjacent non-tumour tissues and the normal oesophageal epithelial cell line HET-1A, respectively. Increased METTL3 expression was associated with an advanced clinical stage of ESCC and poorer prognosis. Furthermore, the genetic knockdown of METTL3 using small interfering RNA significantly suppressed ESCC growth, invasion and migration , and induced cellular apoptosis, in addition to reducing the phosphorylation levels of PI3K and AKT. In conclusion, the present study demonstrated that the upregulation of METTL3 promoted ESCC progression, and that inhibition of METTL3 significantly suppressed the malignant phenotypes of ESCC cells, at least in part, by downregulating PI3K/AKT signalling activity. Thus, it is suggested that METTL3 may be a promising therapeutic target for ESCC.