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Nuclear Localization of Fibroblast Growth Factor Receptor 1 in Breast Cancer Cells Interacting with Cancer Associated Fibroblasts
DC Field | Value | Language |
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dc.contributor.author | Suh, Jinyoung | - |
dc.contributor.author | Kim, Do-Hee | - |
dc.contributor.author | Kim, Su-Jung | - |
dc.contributor.author | Cho, Nam-Chul | - |
dc.contributor.author | Lee, Yeon-Hwa | - |
dc.contributor.author | Jang, Jeong-Hoon | - |
dc.contributor.author | Surh, Young-Joon | - |
dc.date.accessioned | 2022-06-24T01:16:03Z | - |
dc.date.available | 2022-06-24T01:16:03Z | - |
dc.date.created | 2022-05-16 | - |
dc.date.created | 2022-05-16 | - |
dc.date.issued | 2022-03 | - |
dc.identifier.citation | 대한암예방학회지, Vol.27 No.1, pp.68-76 | - |
dc.identifier.issn | 2288-3649 | - |
dc.identifier.uri | https://hdl.handle.net/10371/183965 | - |
dc.description.abstract | Cancer-associated fibroblasts (CAFs) represent a major component of the tumor microenvironment and interplay with cancer cells by secreting cytokines, growth factors and extracellular matrix proteins. When estrogen receptor-negative breast cancer MDA-MB-231 cells were treated with the CAF-conditioned medium (CAF-CM), Akt and STAT3 involved in cell proliferation and survival were activated through phosphorylation. CAFs secrete fibroblast growth factor 2 (FGF2), thereby stimulating breast cancer cell progression. Akt activation induced by CAF-CM in MDA-MB-231 cells was abolished when FGF2-neutralizing antibody was added. Treatment of MDA-MB-231 cells directly with FGF2 enhanced the phosphorylation of Akt and the FGF receptor (FGFR) substrate, FRS2a. These events were abrogated by siRNA-mediated silencing of FGFR1. In a xenograft mouse model, co-injection of MDA-MB-231 cells with activated fibroblasts expressing FGF2 dramatically enhanced activation of Akt. Stable knockdown of FGFR1 blunted Akt phosphorylation in xenograft tumors. MDA-MB-231 cells co-cultured with CAFs or directly stimulated with FGF2 exhibited enhanced nuclear localization of FGFR1. Notably, FGF2 stimulation produced reactive oxygen species (ROS) accumulation in MDA-MB-231 cells, and FGF2-induced nuclear accumulation of FGFR1 was abrogated by the ROS scavenging agent, N-acetylcysteine. | - |
dc.language | 영어 | - |
dc.publisher | 대한암예방학회 | - |
dc.title | Nuclear Localization of Fibroblast Growth Factor Receptor 1 in Breast Cancer Cells Interacting with Cancer Associated Fibroblasts | - |
dc.type | Article | - |
dc.citation.journaltitle | 대한암예방학회지 | - |
dc.identifier.wosid | 000788271100002 | - |
dc.citation.endpage | 76 | - |
dc.citation.number | 1 | - |
dc.citation.startpage | 68 | - |
dc.citation.volume | 27 | - |
dc.identifier.kciid | ART002829253 | - |
dc.description.isOpenAccess | Y | - |
dc.contributor.affiliatedAuthor | Surh, Young-Joon | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.subject.keywordPlus | EGF RECEPTOR | - |
dc.subject.keywordPlus | FGFR1 | - |
dc.subject.keywordPlus | TRANSLOCATION | - |
dc.subject.keywordPlus | TRAFFICKING | - |
dc.subject.keywordPlus | NRF2 | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | TRANSPORT | - |
dc.subject.keywordPlus | INVASION | - |
dc.subject.keywordPlus | HEPARIN | - |
dc.subject.keywordPlus | BINDING | - |
dc.subject.keywordAuthor | Breast cancer | - |
dc.subject.keywordAuthor | Cancer-associated fibroblasts | - |
dc.subject.keywordAuthor | Fibroblast growth factor 2 | - |
dc.subject.keywordAuthor | Fibroblast growth factor receptor 1 | - |
dc.subject.keywordAuthor | Tumor microenvironment | - |
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