Antitumor effects of metformin are a result of inhibiting nuclear factor kappa B nuclear translocation in esophageal squamous cell carcinoma
| العنوان: | Antitumor effects of metformin are a result of inhibiting nuclear factor kappa B nuclear translocation in esophageal squamous cell carcinoma |
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| المؤلفون: | Kentaro Murakami, Yasunori Matsumoto, Takeshi Toyozumi, Isamu Hoshino, Hisahiro Matsubara, Yasunori Akutsu, Ryota Otsuka, Tadashi Shiraishi, Naoyuki Hanari, Keiko Iida, Koichiro Okada, Aki Komatsu Akimoto, Haruhito Sakata, Masaya Yokoyama, Masahiko Takahashi, Masayuki Kano, Nobufumi Sekino |
| المصدر: | Cancer Science |
| بيانات النشر: | John Wiley and Sons Inc., 2018. |
| سنة النشر: | 2018 |
| مصطلحات موضوعية: | 0301 basic medicine, Cancer Research, Combination therapy, endocrine system diseases, Esophageal Neoplasms, Mice, Nude, Antineoplastic Agents, Apoptosis, Translocation, Genetic, 03 medical and health sciences, Mice, 0302 clinical medicine, Cell, Molecular, and Stem Cell Biology, Cell Movement, Cell Line, Tumor, medicine, Animals, Humans, Cell Lineage, Epithelial–mesenchymal transition, Transcription factor, Cell Nucleus, Inflammation, Mice, Inbred BALB C, epithelial‐mesenchymal transition, business.industry, NF-kappa B, Cancer, nutritional and metabolic diseases, General Medicine, Original Articles, NFKB1, medicine.disease, Cadherins, Metformin, esophageal squamous cell carcinoma, 030104 developmental biology, Oncology, Diabetes Mellitus, Type 2, Cell culture, 030220 oncology & carcinogenesis, Cancer research, treatment outcome, Carcinoma, Squamous Cell, Original Article, business, medicine.drug |
| الوصف: | 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. |
| اللغة: | English |
| تدمد: | 1349-7006 1347-9032 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c8f35973239cfc96bb9faf8aa36b46da http://europepmc.org/articles/PMC5891201 |
| حقوق: | OPEN |
| رقم الأكسشن: | edsair.doi.dedup.....c8f35973239cfc96bb9faf8aa36b46da |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 13497006 13479032 |
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