UBE2T promotes epithelial‑mesenchymal transition and motility in oral cancer cells via induction of IL‑6 expression

Abstract

Oral squamous cell carcinoma (OSCC) is a prevalent aggressive malignancy with a high mortality rate. However, the mechanisms underlying the progression of OSCC remain to be elucidated. In the present study, bioinformatics analysis identified ubiquitin‑conjugating enzyme E2 T (UBE2T) as a poor prognostic factor in head and neck cancer, showing the strongest association with cancer stage progression. Functional studies revealed that UBE2T can enhance motility and induce epithelial‑mesenchymal transition (EMT) in OSCC cells. RNA sequencing and subsequent analyses demonstrated that UBE2T upregulated the expression levels of various motility‑ and EMT‑related factors, including ankyrin repeat domain 1, endothelin‑1, interleukin‑6 (IL‑6), matrix metal‑ loproteinase‑9 and plasminogen activator, urokinase. Gene set enrichment analysis indicated that UBE2T activates the IL‑6/Janus protein tyrosine kinase (JAK)/signal transducer and activator of transcription 3 signaling pathway. Moreover, treatment of OSCC cells with IL‑6 or a JAK inhibitor resulted in the induction of EMT and mesenchymal‑epithelial transi‑ tion, respectively, accompanied by enhanced and suppressed cancer cell motility. These results indicated that IL‑6, which is upregulated by UBE2T, may be crucial for maintaining mesenchymal traits and motility in OSCC cells. Collectively, these findings suggested that the UBE2T/IL‑6/JAK axis may serve as a potential therapeutic target for OSCC.