https://scholars.lib.ntu.edu.tw/handle/123456789/473330
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.author | Huang C.-K. | en_US |
dc.contributor.author | Yang C.-Y. | en_US |
dc.contributor.author | YUNG-MING JENG | en_US |
dc.contributor.author | Chen C.-L. | en_US |
dc.contributor.author | Wu H.-H. | en_US |
dc.contributor.author | YI-CHENG CHANG | en_US |
dc.contributor.author | Ma C. | en_US |
dc.contributor.author | WEN-HUNG KUO | en_US |
dc.contributor.author | KING-JEN CHANG | en_US |
dc.contributor.author | Shew J.-Y. | en_US |
dc.contributor.author | Lee W.-H. | en_US |
dc.creator | Huang C.-K.;Yang C.-Y.;Yung-Ming Jeng;Chen C.-L.;Wu H.-H.;Chang Y.-C.;Ma C.;Kuo W.-H.;Chang K.-J.;Shew J.-Y.;Lee W.-H. | - |
dc.date.accessioned | 2020-03-06T08:25:04Z | - |
dc.date.available | 2020-03-06T08:25:04Z | - |
dc.date.issued | 2014 | - |
dc.identifier.issn | 0950-9232 | - |
dc.identifier.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-84902135400&doi=10.1038%2fonc.2013.268&partnerID=40&md5=4a8e787b39099060ee70fe40a4a1e8a2 | - |
dc.identifier.uri | https://scholars.lib.ntu.edu.tw/handle/123456789/473330 | - |
dc.description.abstract | Gain of function of membrane receptor was a good strategy exploited by cancer cells to benefit own growth and survival. Overexpression of HER2 has been found to serve as a target for developing trastuzumab to treat 20-25% of breast cancer. However, little or none of the other membrane receptor was found to be useful as a potential target for breast cancer treatment since then. Here, we showed that amplified signaling of interleukin-17 receptor B (IL-17RB) and its ligand IL-17B promoted tumorigenicity in breast cancer cells and impeded acinus formation in immortalized normal mammary epithelial cells. External signal transmitted through IL-17RB activated nuclear factor-κB to upregulate antiapoptotic factor Bcl-2 and induced etoposide resistance. Elevated expression of IL-17RB had a stronger correlation with poor prognosis than HER2 in breast cancer patients. Interestingly, breast cancer patients with high expression of IL-17RB and HER2 had the shortest survival rate. Depletion of IL-17RB in trastuzumab-resistant breast cancer cells significantly reduced their tumorigenic activity, suggesting that IL-17RB and HER2 have an independent role in breast carcinogenesis. Furthermore, treatment with antibodies specifically against IL-17RB or IL-17B effectively attenuated tumorigenicity of breast cancer cells. These results suggest that the amplified IL-17RB/IL-17B signaling pathways may serve as a therapeutic target for developing treatment to manage IL-17RB-Associated breast cancer.. ? 2014 Macmillan Publishers Limited All rights reserved 0950-9232/14. | - |
dc.publisher | Nature Publishing Group | - |
dc.relation.ispartof | Oncogene | - |
dc.subject.classification | [SDGs]SDG3 | - |
dc.subject.other | caspase 3; epidermal growth factor receptor; epidermal growth factor receptor 2; etoposide; immunoglobulin enhancer binding protein; interleukin 17 receptor; interleukin 17b receptor; protein bcl 2; survivin; trastuzumab; tumor necrosis factor receptor associated factor 6; unclassified drug; X linked inhibitor of apoptosis; acinar cell; anchorage independent growth; apoptosis; article; breast cancer; breast carcinogenesis; breast epithelium; cancer cell; cancer growth; cancer prognosis; cancer resistance; cancer size; cancer survival; carcinogenic activity; controlled study; enzyme activation; gene amplification; human; human cell; priority journal; protein depletion; protein expression; signal transduction; upregulation; Animals; Apoptosis; Autocrine Communication; Breast Neoplasms; Carcinogenesis; Cell Line, Tumor; Etoposide; Female; Gene Expression Regulation, Neoplastic; Humans; Interleukin-17; Mammary Neoplasms, Experimental; MCF-7 Cells; Mice; Mice, Inbred NOD; Mice, SCID; NF-kappa B; Paracrine Communication; Receptor, erbB-2; Receptors, Interleukin-17; Signal Transduction; Xenograft Model Antitumor Assays | - |
dc.title | Autocrine/paracrine mechanism of interleukin-17B receptor promotes breast tumorigenesis through NF-κB-mediated antiapoptotic pathway | en_US |
dc.type | journal article | en |
dc.identifier.doi | 10.1038/onc.2013.268 | - |
dc.identifier.pmid | 23851503 | - |
dc.identifier.scopus | 2-s2.0-84902135400 | - |
dc.relation.pages | 2968-2977 | - |
dc.relation.journalvolume | 33 | - |
dc.relation.journalissue | 23 | - |
item.openairecristype | http://purl.org/coar/resource_type/c_6501 | - |
item.openairetype | journal article | - |
item.grantfulltext | none | - |
item.cerifentitytype | Publications | - |
item.fulltext | no fulltext | - |
crisitem.author.dept | Pathology | - |
crisitem.author.dept | Pathology-NTUH | - |
crisitem.author.dept | Medical Genomics and Proteomics | - |
crisitem.author.dept | Internal Medicine | - |
crisitem.author.dept | Internal Medicine-NTUH | - |
crisitem.author.dept | Surgery-NTUH | - |
crisitem.author.dept | Surgery | - |
crisitem.author.dept | Surgery | - |
crisitem.author.dept | Surgery-NTUH | - |
crisitem.author.orcid | 0000-0002-3878-4491 | - |
crisitem.author.orcid | 0000-0002-8077-5011 | - |
crisitem.author.orcid | 0000-0002-9881-4605 | - |
crisitem.author.orcid | 0000-0001-9811-3422 | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
顯示於: | 病理學科所 |
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