HOXC6 Activates BCAT1 Expression to Promote Oral Cancer Development

This paper aims to reveal the impact of HOXC6 on oral cancer development through the regulation of BCAT1 and the molecular mechanism.

BCAT1 expression in oral cancer tissues and adjacent tissues was verified by western blot analysis and RT-qPCR. After knocking down BCAT1, the HN6 and HN30 cell proliferation, migration, invasion, and apoptosis were detected. The upstream mechanism of BCAT1 elevation was investigated by bioinformatics analysis. HOXC6 expression was detected by immunohistochemistry in oral cancer and adjacent tissues. ChIP and dual-luciferase assay were used to detect the interaction between HOXC6 and the BCAT1 promoter. Rescue experiments were carried out to substantiate the malignant phenotype and epithelial-to-mesenchymal transition (EMT) of oral cancer cells. An in vivo xenograft tumor model was constructed.

BCAT1 and HOXC6 were abnormally high in oral cancer tissues. Inhibition of BCAT1 suppressed the proliferation, migration, invasion, and EMT, and promoted apoptosis of oral cancer cells. HOXC6 downregulation curbed the malignant behavior and EMT program of oral cancer cells. HOXC6 was enriched in the BCAT1 promoter in oral cancer cells. HOXC6 silencing downregulated BCAT1 expression. Transcriptional activation of BCAT1 by HOXC6 promoted oral cancer progression.

HOXC6 knockdown inhibits BCAT1 expression to suppress oral cancer development.