Epithelial-mesenchymal transition (EMT) serves an important role in the formation and development of various types of
cancer, including
oral squamous cell carcinoma (OSCC).
Metformin, used for treating
type 2 diabetes, has been revealed to exert an anticancer effect in various types of
cancer, including liver, breast and
colorectal cancer. However, its role in the EMT of OSCC has been rarely reported. Therefore, the present study aimed to investigate the effects of
metformin on EMT and to identify its underlying mechanism in OSCC. Firstly, EMT was induced in CAL-27 cells using CoCl2. Subsequently, the effects of
metformin on cell viability, migration and xenograft growth were evaluated in vitro and in vivo. Reverse transcription-quantitative PCR was performed to detect the expression levels of
E-cadherin,
vimentin, snail family transcriptional repressor 1, mTOR,
hypoxia inducible factor 1α,
pyruvate kinase M2 and STAT3. The results demonstrated that
metformin abolished CoCl2-induced cell proliferation, migration, invasion and EMT. Moreover,
metformin reversed EMT in OSCC by inhibiting the mTOR-associated HIF-1α/PKM2/STAT3 signaling pathway. Overall, the present findings characterized a novel mechanism via which
metformin modulated EMT in OSCC.