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Esophageal squamous cell carcinoma ( ESCC ) is an intractable digestive organ cancer that has proven difficult to treat despite multidisciplinary therapy, and a new treatment strategy is demanded. Metformin is used for type 2 diabetes mellitus and its antitumor effects have been reported recently. Metformin exerts antitumor effects in various respects, such as inhibiting inflammation, tumor growth and epithelial‐mesenchymal transition ( EMT ). However, few reports have described the efficacy of metformin on  ESCC , and their findings have been controversial. We analyzed the antitumor effects of metformin and clarified its effects on anti‐inflammation, growth suppression and  EMT  inhibition. Activation of nuclear factor kappa B ( NF ‐κB), the major transcription factor induced by inflammation, was investigated by immunostaining. We found that localization of  NF ‐κB in the nucleus was reduced after metformin treatment. This suggests that metformin inhibited the activation of  NF ‐κB. Metformin inhibited tumor growth and induced apoptosis in  ESCC  cell lines. Associated with  EMT , we examined cell motility by a wound healing assay and the epithelial marker E‐cadherin expression of various  ESCC  cell lines by western blotting. Metformin inhibited cell motility and induced E‐cadherin expression. In conclusion, metformin showed multiple antitumor effects such as growth suppression, invasion inhibition, and control of  EMT  by inhibiting  NF ‐κB localization on  ESCC . Further exploration of the marker of treatment efficacy and combination therapy could result in the possibility for novel treatment to use metformin on  ESCC .

Antitumor effects of metformin are a result of inhibiting nuclear factor kappa B nuclear translocation in esophageal squamous cell carcinoma