Branched chain amino acid transaminase 1 (BCAT1) overexpression has been reported in various cancers; however, at present, its significance and biological role in head and neck squamous cell carcinoma (HNSCC) remain unknown. BCAT1 protein expression was upregulated in 56/106 (52.8%) cases of HNSCC. BCAT1 overexpression was associated with tumor-node-metastasis stage, tumor stage and nodal metastasis. The Cancer Genome Atlas data suggested that high BCAT1 expression was associated with poor patient survival. Oncomine data suggested that BCAT1 expression was increased in HNSCC. Functionally, BCAT1 overexpression promoted cell proliferation, colony formation, invasion and cisplatin resistance in FaDu cells. BCAT1 overexpression also upregulated the mitochondrial membrane potential, and increased ATP production, glucose consumption and glucose uptake. Western blotting demonstrated that BCAT1 overexpression upregulated c-Myc and glucose transporter 1 (GLUT1) protein levels. Depletion of c-Myc using small interfering RNA abolished the influence of BCAT1 on GLUT1. Chromatin immunoprecipitation assays demonstrated that c-Myc has binding sites in the GLUT1 promoter. Collectively, the present findings suggested that BCAT1 is upregulated in human HNSCC and regulates HNSCC cell proliferation, invasion, cisplatin sensitivity and c-Myc/GLUT1 signaling.

Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is involved in the oncogenesis and progression of various types of cancer. However, the function of MALAT1 in hypopharyngeal squamous cell carcinoma (HSCC) is not completely understood. In the present study, MALAT1 expression levels were determined using reverse transcription-quantitative PCR, and Cell Counting Kit-8, Transwell and flow cytometry assays were performed to investigate the biological functions of HSCC cells. The results indicated that MALAT1 was upregulated in HSCC. MALAT1 knockdown suppressed HSCC cell proliferation, migration and invasion, and promoted apoptosis compared with the control group. Additionally, microRNA (miR)-194 was identified as a target of MALAT1 and was expressed at low levels in HSCC tissues compared with adjacent non-tumor tissues. A miR-194 agomir inhibited malignant cell behaviors, including cell proliferation, migration and invasion, whereas miR-194 antagomir promoted malignant behaviors compared with the corresponding control groups. In addition, the results suggested that MALAT1 knockdown inhibited the malignant behaviors of HSCC cells by binding miR-194. miR-194 inhibition partially reversed the MALAT1 knockdown-induced inhibitory effects on HSCC cells. Furthermore, MALAT1 knockdown combined with miR194 mimics resulted in the lowest tumor volume among all tested groups in vivo. In conclusion, the results of the present study suggested that MALAT1 knockdown suppressed the malignant behavior of HSCC by targeting miR-194; therefore, MALAT1 may serve as a novel therapeutic target for HSCC.