Therapeutic potential of metformin in papillary thyroid cancer in vitro and in vivo
DC Field | Value | Language |
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dc.contributor.author | Cho, Sun Wook | - |
dc.contributor.author | Yi, Ka Hee | - |
dc.contributor.author | Han, Sun Kyoung | - |
dc.contributor.author | Sun, Hyun Jin | - |
dc.contributor.author | Kim, Ye An | - |
dc.contributor.author | Oh, Byung-Chul | - |
dc.contributor.author | Park, Young Joo | - |
dc.contributor.author | Park, Do Joon | - |
dc.date.available | 2020-02-28T16:44:40Z | - |
dc.date.created | 2020-02-06 | - |
dc.date.issued | 2014-08-05 | - |
dc.identifier.issn | 0303-7207 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/12369 | - |
dc.description.abstract | Metformin, an anti-diabetic drug used in type 2 diabetes treatment, is reported to have oncopreventive or therapeutic roles in several human cancers. The present study investigated the therapeutic. potential of physiologic dose of metformin in PTC. Metformin inhibited PTC cell viability and increased cell apoptosis in various doses (0.5-20 mM) in BCPAP and BHP10-3SC cells. Western blot analysis demonstrated that the p-AMPK/AMPK ratio increased with increased metformin treatment. The ectopic tumor experiment was performed using BHP10-3SC cells and athymic nude mice. Oral metformin treatment via drinking water significantly delayed tumor growth in both tumor development model and established tumor models. Necrotic area in tumors significantly increased with metformin treatment. Western blot analysis revealed an increase in p-AMPK/AMPK ratio and suppressions of mTOR and Akt expressions in metformin-treated mice compared to the results in mock-treated control mice. Our results indicate that a physiologic dose of metformin has anti-tumorigenic effects that result from activation of AMPK signaling and Inhibition of Akt signaling. (C) 2014 Elsevier Ireland Ltd. All rights reserved. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | ELSEVIER IRELAND LTD | - |
dc.relation.isPartOf | MOLECULAR AND CELLULAR ENDOCRINOLOGY | - |
dc.subject | ATHYMIC NUDE-MICE | - |
dc.subject | BREAST-CANCER | - |
dc.subject | DIABETIC-PATIENTS | - |
dc.subject | INSULIN-RESISTANCE | - |
dc.subject | INHIBITS GROWTH | - |
dc.subject | CARCINOMA | - |
dc.subject | CELLS | - |
dc.subject | NEOADJUVANT | - |
dc.subject | RECEPTORS | - |
dc.subject | APOPTOSIS | - |
dc.title | Therapeutic potential of metformin in papillary thyroid cancer in vitro and in vivo | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000341468700004 | - |
dc.identifier.doi | 10.1016/j.mce.2014.05.021 | - |
dc.identifier.bibliographicCitation | MOLECULAR AND CELLULAR ENDOCRINOLOGY, v.393, no.1-2, pp.24 - 29 | - |
dc.identifier.scopusid | 2-s2.0-84902456668 | - |
dc.citation.endPage | 29 | - |
dc.citation.startPage | 24 | - |
dc.citation.title | MOLECULAR AND CELLULAR ENDOCRINOLOGY | - |
dc.citation.volume | 393 | - |
dc.citation.number | 1-2 | - |
dc.contributor.affiliatedAuthor | Oh, Byung-Chul | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | Metformin | - |
dc.subject.keywordAuthor | AMPK | - |
dc.subject.keywordAuthor | Akt | - |
dc.subject.keywordAuthor | Papillary thyroid cancer (PTC) | - |
dc.subject.keywordAuthor | Ectopic tumor | - |
dc.subject.keywordAuthor | Mouse | - |
dc.subject.keywordPlus | ATHYMIC NUDE-MICE | - |
dc.subject.keywordPlus | BREAST-CANCER | - |
dc.subject.keywordPlus | DIABETIC-PATIENTS | - |
dc.subject.keywordPlus | INSULIN-RESISTANCE | - |
dc.subject.keywordPlus | INHIBITS GROWTH | - |
dc.subject.keywordPlus | CARCINOMA | - |
dc.subject.keywordPlus | CELLS | - |
dc.subject.keywordPlus | NEOADJUVANT | - |
dc.subject.keywordPlus | RECEPTORS | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalResearchArea | Endocrinology & Metabolism | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Endocrinology & Metabolism | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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