Maackia amurensis seed lectin inhibits oral squamous cell carcinoma tumorigenesis by suppressing N6-methyladenosine modification-mediated SRY-box transcription factor 2 expression.

ObjectiveStudies have indicated that combining Maackia amurensis seed lectin with first-line chemotherapeutic agents enhances the efficacy of treatment for oral squamous cell carcinoma. The study aimed to investigate the underlying mechanism of Maackia amurensis seed lectin in the treatment of oral squamous cell carcinoma.MethodsGene Expression Omnibus dataset mining, reverse transcription-quantitative polymerase chain reaction, and western blot analysis were performed to identify the expression of SRY-box transcription factor 2, methyltransferase 3, and YTH domain-containing protein 1 in oral squamous cell carcinoma. The N6-methyladenosine methylation levels of SRY-box transcription factor 2 were detected though methylated RNA immunoprecipitation. The effects of Maackia amurensis seed lectin and SRY-box transcription factor 2 on oral squamous cell carcinoma cells were determined via Cell Counting Kit-8 and colony formation assays.ResultsThe results demonstrated that increased expression of SRY-box transcription factor 2 in oral squamous cell carcinoma is correlated with elevated levels of N6-methyladenosine modification, and treatment with Maackia amurensis seed lectin reduces the N6-methyladenosine modification level and SRY-box transcription factor 2 expression. Moreover, overexpression of SRY-box transcription factor 2 reversed the inhibitory effects of Maackia amurensis seed lectin on oral squamous cell carcinoma cell proliferation and colony formation.ConclusionsMaackia amurensis seed lectin may inhibit oral squamous cell carcinoma cell proliferation by suppressing N6-methyladenosine modification-mediated SRY-box transcription factor 2 expression, thereby improving chemotherapy sensitivity in oral squamous cell carcinoma.