The novel IGF-IR/Akt-dependent anticancer activities of glucosamine
DC Field | Value | Language |
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dc.contributor.author | Song, Ki-Hoon | - |
dc.contributor.author | Kang, Ju-Hee | - |
dc.contributor.author | Woo, Jong-Kyu | - |
dc.contributor.author | Nam, Jeong-Seok | - |
dc.contributor.author | Min, Hye-Young | - |
dc.contributor.author | Lee, Ho-Young | - |
dc.contributor.author | Kim, Soo-Youl | - |
dc.contributor.author | Oh, Seung-Hyun | - |
dc.date.available | 2020-02-28T18:42:58Z | - |
dc.date.created | 2020-02-06 | - |
dc.date.issued | 2014-01-20 | - |
dc.identifier.issn | 1471-2407 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/12896 | - |
dc.description.abstract | Background: Recent studies have shown that glucosamine inhibits the proliferation of various human cancer cell lines and downregulates the activity of COX-2, HIF-1 alpha, p70S6K, and transglutaminase 2. Because the IGF-1R/Akt pathway is a common upstream regulator of p70S6K, HIF-1 alpha, and COX-2, we hypothesized that glucosamine inhibits cancer cell proliferation through this pathway. Methods: We used various in vitro assays including flow cytometry assays, small interfering RNA (siRNA) transfection, western blot analysis, MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assays, reverse transcription-polymerase chain reaction, and in vivo xenograft mouse model to confirm anticancer activities of glucosamine and to investigate the molecular mechanism. Results: We found that glucosamine inhibited the growth of human non-small cell lung cancer (NSCLC) cells and negatively regulated the expression of IGF-1R and phosphorylation of Akt. Glucosamine decreased the stability of IGF-1R and induced its proteasomal degradation by increasing the levels of abnormal glycosylation on IGF-1R. Moreover, picropodophyllin, a selective inhibitor of IGF-1R, and the IGF-1R blocking antibody IMC-A12 induced significant cell growth inhibition in glucosamine-sensitive, but not glucosamine-resistant cell lines. Using in vivo xenograft model, we confirmed that glucosamine prohibits primary tumor growth through reducing IGF-1R signalling and increasing ER-stress. Conclusions: Taken together, our results suggest that targeting the IGF-1R/Akt pathway with glucosamine may be an effective therapeutic strategy for treating some type of cancer. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | BIOMED CENTRAL LTD | - |
dc.relation.isPartOf | BMC CANCER | - |
dc.subject | PROSTATE-CANCER CELLS | - |
dc.subject | ASCITES TUMOR CELLS | - |
dc.subject | SELECTIVE-INHIBITION | - |
dc.subject | CARCINOMA-CELLS | - |
dc.subject | DOWN-REGULATION | - |
dc.subject | LEUKEMIC-CELLS | - |
dc.subject | PROTEIN | - |
dc.subject | PATHWAY | - |
dc.subject | GLYCOSYLATION | - |
dc.subject | GROWTH | - |
dc.title | The novel IGF-IR/Akt-dependent anticancer activities of glucosamine | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000331089700001 | - |
dc.identifier.doi | 10.1186/1471-2407-14-31 | - |
dc.identifier.bibliographicCitation | BMC CANCER, v.14 | - |
dc.identifier.scopusid | 2-s2.0-84892455034 | - |
dc.citation.title | BMC CANCER | - |
dc.citation.volume | 14 | - |
dc.contributor.affiliatedAuthor | Woo, Jong-Kyu | - |
dc.contributor.affiliatedAuthor | Nam, Jeong-Seok | - |
dc.contributor.affiliatedAuthor | Oh, Seung-Hyun | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | Glucosamine | - |
dc.subject.keywordAuthor | Anticancer agent | - |
dc.subject.keywordAuthor | IGF-1R | - |
dc.subject.keywordAuthor | Akt | - |
dc.subject.keywordAuthor | Glycosylation | - |
dc.subject.keywordAuthor | ER-stress | - |
dc.subject.keywordPlus | PROSTATE-CANCER CELLS | - |
dc.subject.keywordPlus | ASCITES TUMOR CELLS | - |
dc.subject.keywordPlus | SELECTIVE-INHIBITION | - |
dc.subject.keywordPlus | CARCINOMA-CELLS | - |
dc.subject.keywordPlus | DOWN-REGULATION | - |
dc.subject.keywordPlus | LEUKEMIC-CELLS | - |
dc.subject.keywordPlus | PROTEIN | - |
dc.subject.keywordPlus | PATHWAY | - |
dc.subject.keywordPlus | GLYCOSYLATION | - |
dc.subject.keywordPlus | GROWTH | - |
dc.relation.journalResearchArea | Oncology | - |
dc.relation.journalWebOfScienceCategory | Oncology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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