Combinatorial TGF-beta attenuation with paclitaxel inhibits the epithelial-to-mesenchymal transition and breast cancer stem-like cells
DC Field | Value | Language |
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dc.contributor.author | Park, So-Yeon | - |
dc.contributor.author | Kim, Min-Jin | - |
dc.contributor.author | Park, Sang-A | - |
dc.contributor.author | Kim, Jung-Shin | - |
dc.contributor.author | Min, Kyung-Nan | - |
dc.contributor.author | Kim, Dae-Kee | - |
dc.contributor.author | Lim, Woosung | - |
dc.contributor.author | Nam, Jeong-Seok | - |
dc.contributor.author | Sheen, Yhun Yhong | - |
dc.date.available | 2020-02-28T07:43:11Z | - |
dc.date.created | 2020-02-06 | - |
dc.date.issued | 2015-11-10 | - |
dc.identifier.issn | 1949-2553 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/9944 | - |
dc.description.abstract | Distant relapse after chemotherapy is an important clinical issue for treating breast cancer patients and results from the development of cancer stem-like cells (CSCs) during chemotherapy. Here we report that blocking epithelial-to-mesenchymal transition (EMT) suppresses paclitaxel-induced CSCs properties by using a MDA-MB-231-xenografted mice model (in vivo), and breast cancer cell lines (in vitro). Paclitaxel, one of the cytotoxic taxane-drugs such as docetaxel, increases mesenchymal markers (Vimentin and Fibronectin) and decreases an epithelial marker (Zo-1). Blocking TGF-beta signaling with the TGF-beta type I receptor kinase (ALK5) inhibitor, EW-7197, suppresses paclitaxel-induced EMT and CSC properties such as mammosphere-forming efficiency (MSFE), aldehyde dehydrogenase (ALDH) activity, CD44(+)/CD24(-) ratio, and pluripotency regulators (Oct4, Nanog, Klf4, Myc, and Sox2). The combinatorial treatment of EW-7197 improves the therapeutic effect of paclitaxel by decreasing the lung metastasis and increasing the survival time in vivo. We confirmed that Snail is increased by paclitaxel-induced intracellular reactive oxygen species (ROS) and EW-7197 suppresses the paclitaxel-induced Snail and EMT by attenuating paclitaxel-induced intracellular ROS. Knock-down of SNAI1 suppresses paclitaxel-induced EMT and CSC properties. These data together suggest that blocking the Snail-induced EMT with the ALK5 inhibitor attenuates metastasis after paclitaxel-therapy and that this combinatorial approach could prove useful in treating breast cancer. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | IMPACT JOURNALS LLC | - |
dc.relation.isPartOf | ONCOTARGET | - |
dc.subject | CARCINOMA CELLS | - |
dc.subject | OVARIAN-CANCER | - |
dc.subject | CHEMORESISTANCE | - |
dc.subject | RESISTANCE | - |
dc.subject | SNAIL | - |
dc.subject | EMT | - |
dc.subject | METASTASIS | - |
dc.subject | ACTIVATION | - |
dc.subject | EXPRESSION | - |
dc.subject | CHEMOTHERAPY | - |
dc.title | Combinatorial TGF-beta attenuation with paclitaxel inhibits the epithelial-to-mesenchymal transition and breast cancer stem-like cells | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000366113200044 | - |
dc.identifier.bibliographicCitation | ONCOTARGET, v.6, no.35, pp.37535 - 37552 | - |
dc.identifier.scopusid | 2-s2.0-84947733386 | - |
dc.citation.endPage | 37552 | - |
dc.citation.startPage | 37535 | - |
dc.citation.title | ONCOTARGET | - |
dc.citation.volume | 6 | - |
dc.citation.number | 35 | - |
dc.contributor.affiliatedAuthor | Nam, Jeong-Seok | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | paclitaxel | - |
dc.subject.keywordAuthor | metastasis | - |
dc.subject.keywordAuthor | Snail | - |
dc.subject.keywordAuthor | epithelial-to-mesenchymal transition (EMT) | - |
dc.subject.keywordAuthor | transforming growth factor-beta (TGF-beta) | - |
dc.subject.keywordPlus | CARCINOMA CELLS | - |
dc.subject.keywordPlus | OVARIAN-CANCER | - |
dc.subject.keywordPlus | CHEMORESISTANCE | - |
dc.subject.keywordPlus | RESISTANCE | - |
dc.subject.keywordPlus | SNAIL | - |
dc.subject.keywordPlus | EMT | - |
dc.subject.keywordPlus | METASTASIS | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | CHEMOTHERAPY | - |
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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