Induction of metastatic potential by TrkB via activation of IL6/JAK2/STAT3 and PI3K/AKT signaling in breast cancer
DC Field | Value | Language |
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dc.contributor.author | Kim, Min Soo | - |
dc.contributor.author | Lee, Won Sung | - |
dc.contributor.author | Jeong, Joon | - |
dc.contributor.author | Kim, Seong-Jin | - |
dc.contributor.author | Jin, Wook | - |
dc.date.available | 2020-02-28T07:42:51Z | - |
dc.date.created | 2020-02-06 | - |
dc.date.issued | 2015-11-24 | - |
dc.identifier.issn | 1949-2553 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/9923 | - |
dc.description.abstract | In metastatic breast cancers, the acquisition of metastatic ability, which leads to clinically incurable disease and poor survival, has been associated with acquisition of epithelial-mesenchymal transition (EMT) program and self-renewing trait (CSCs) via activation of PI3K/AKT and IL6/JAK2/STAT3 signaling pathways. We found that TrkB is a key regulator of PI3K/AKT and JAK/STAT signal pathway-mediated tumor metastasis and EMT program. Here, we demonstrated that TrkB activates AKT by directly binding to c-Src, leading to increased proliferation. Also, TrkB increases Twist-1 and Twist-2 expression through activation of JAK2/STAT3 by inducing c-Src-JAK2 complex formation. Furthermore, TrkB in the absence of c-Src binds directly to JAK2 and inhibits SOCS3-mediated JAK2 degradation, resulting in increased total JAK2 and STAT3 levels, which subsequently leads to JAK2/STAT3 activation and Twist-1 upregulation. Additionally, activation of the JAK2/STAT3 pathway via induction of IL-6 secretion by TrkB enables induction of activation of the EMT program via induction of STAT3 nuclear translocation. These observations suggest that TrkB is a promising target for future intervention strategies to prevent tumor metastasis, EMT program and self-renewing trait in breast cancer. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | IMPACT JOURNALS LLC | - |
dc.relation.isPartOf | ONCOTARGET | - |
dc.subject | EPITHELIAL-MESENCHYMAL TRANSITION | - |
dc.subject | STEM-CELLS | - |
dc.subject | ANOIKIS RESISTANCE | - |
dc.subject | GROWTH-FACTOR | - |
dc.subject | TWIST EXPRESSION | - |
dc.subject | RECEPTOR TRKB | - |
dc.subject | UP-REGULATION | - |
dc.subject | SRC | - |
dc.subject | STAT3 | - |
dc.subject | IL-6 | - |
dc.title | Induction of metastatic potential by TrkB via activation of IL6/JAK2/STAT3 and PI3K/AKT signaling in breast cancer | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000366114400060 | - |
dc.identifier.doi | 10.18632/oncotarget.5522 | - |
dc.identifier.bibliographicCitation | ONCOTARGET, v.6, no.37, pp.40158 - 40171 | - |
dc.identifier.scopusid | 2-s2.0-84950161335 | - |
dc.citation.endPage | 40171 | - |
dc.citation.startPage | 40158 | - |
dc.citation.title | ONCOTARGET | - |
dc.citation.volume | 6 | - |
dc.citation.number | 37 | - |
dc.contributor.affiliatedAuthor | Kim, Min Soo | - |
dc.contributor.affiliatedAuthor | Jin, Wook | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | TrkB | - |
dc.subject.keywordAuthor | epithelial-mesenchymal transition (EMT) | - |
dc.subject.keywordAuthor | IL-6/JAK2/STAT3 pathway | - |
dc.subject.keywordAuthor | PI3K/AKT pathway | - |
dc.subject.keywordAuthor | metastasis and tumorigenicity | - |
dc.subject.keywordPlus | EPITHELIAL-MESENCHYMAL TRANSITION | - |
dc.subject.keywordPlus | STEM-CELLS | - |
dc.subject.keywordPlus | ANOIKIS RESISTANCE | - |
dc.subject.keywordPlus | GROWTH-FACTOR | - |
dc.subject.keywordPlus | TWIST EXPRESSION | - |
dc.subject.keywordPlus | RECEPTOR TRKB | - |
dc.subject.keywordPlus | UP-REGULATION | - |
dc.subject.keywordPlus | SRC | - |
dc.subject.keywordPlus | STAT3 | - |
dc.subject.keywordPlus | IL-6 | - |
dc.relation.journalResearchArea | Oncology | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Oncology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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