S100A4 negatively regulates beta-catenin by inducing the Egr-1-PTEN-Akt-GSK3 beta degradation pathway
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Yang, Wonseok | - |
dc.contributor.author | Nam, KeeSoo | - |
dc.contributor.author | Ju, Ji-hyun | - |
dc.contributor.author | Lee, Kyung-min | - |
dc.contributor.author | Oh, Sunhwa | - |
dc.contributor.author | Shin, Incheol | - |
dc.date.accessioned | 2022-07-07T13:28:40Z | - |
dc.date.available | 2022-07-07T13:28:40Z | - |
dc.date.created | 2021-05-12 | - |
dc.date.issued | 2014-10 | - |
dc.identifier.issn | 0898-6568 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/144492 | - |
dc.description.abstract | S100A4, also known as the mts1 gene, has been reported as an invasive and metastatic marker for many types of cancers. S100A4 interacts with various target genes that affect tumor cell metastasis; however, little is known about cellular signaling pathways elicited by S100A4. In the current study, we demonstrate an inhibitory effect of S100A4 on beta-catenin signaling in breast cancer cells. By overexpressing S100A4 in MCF-7, MDA-MB-231 and MDA-MB-453 breast cancer cells, we observed the down-regulation of beta-catenin expression and beta-catenin-dependent TCF/LEF transcriptional activities. The activity of GSK3 beta, which phosphorylates beta-catenin and induces proteasomal degradation of beta-catenin, was increased in S100A4-overexpressing cell lines. Blocking Glycogen Synthase Kinase (GSK3 beta) activity by lithium chloride or Dvl gene overexpression restored beta-catenin expression. We also found that increased GSK3 beta activity was due to decrease in Ala activity resulting from Egr-1-induced phosphatase and tensin homolog (PTEN) expression. S100A4 induced Egr-1 nuclear localization by increasing the association between Egr-1 and importin-7 and this effect was reduced in S100A4 mutants that harbored a defect in nuclear localization signals. Collectively, we verify herein that S100A4 may act as a tumor suppressor in breast cancers by down-regulating the central signaling axis for tumor cell survival. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | ELSEVIER SCIENCE INC | - |
dc.title | S100A4 negatively regulates beta-catenin by inducing the Egr-1-PTEN-Akt-GSK3 beta degradation pathway | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Shin, Incheol | - |
dc.identifier.doi | 10.1016/j.cellsig.2014.06.007 | - |
dc.identifier.scopusid | 2-s2.0-84904434398 | - |
dc.identifier.wosid | 000340983200003 | - |
dc.identifier.bibliographicCitation | CELLULAR SIGNALLING, v.26, no.10, pp.2096 - 2106 | - |
dc.relation.isPartOf | CELLULAR SIGNALLING | - |
dc.citation.title | CELLULAR SIGNALLING | - |
dc.citation.volume | 26 | - |
dc.citation.number | 10 | - |
dc.citation.startPage | 2096 | - |
dc.citation.endPage | 2106 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.subject.keywordPlus | EPITHELIAL-MESENCHYMAL TRANSITION | - |
dc.subject.keywordPlus | GLYCOGEN-SYNTHASE KINASE-3 | - |
dc.subject.keywordPlus | EGR-1 TRANSCRIPTION FACTOR | - |
dc.subject.keywordPlus | CALCIUM-BINDING PROTEIN | - |
dc.subject.keywordPlus | SIGNALING PATHWAY | - |
dc.subject.keywordPlus | COLON-CANCER | - |
dc.subject.keywordPlus | CARCINOMA-CELLS | - |
dc.subject.keywordPlus | METASTASIS | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | PHOSPHORYLATION | - |
dc.subject.keywordAuthor | S100A4 | - |
dc.subject.keywordAuthor | beta-Catenin | - |
dc.subject.keywordAuthor | Egr-1 | - |
dc.subject.keywordAuthor | Akt | - |
dc.subject.keywordAuthor | Breast cancer | - |
dc.identifier.url | https://www.sciencedirect.com/science/article/pii/S0898656814002022?via%3Dihub | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
222, Wangsimni-ro, Seongdong-gu, Seoul, 04763, Korea+82-2-2220-1365
COPYRIGHT © 2021 HANYANG UNIVERSITY.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.