https://scholars.lib.ntu.edu.tw/handle/123456789/346264
DC 欄位 | 值 | 語言 |
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dc.contributor.author | KENG-HSUEH LAN | en |
dc.creator | Neal, C.L.;Yao, J.;Yang, W.;Zhou, X.;Nguyen, N.T.;Lu, J.;Danes, C.G.;Guo, H.;Lan, K.-H.;Ensor, J.;Hittelman, W.;Hung, M.-C.;Yu, D. | - |
dc.date.accessioned | 2018-09-10T07:24:55Z | - |
dc.date.available | 2018-09-10T07:24:55Z | - |
dc.date.issued | 2009 | - |
dc.identifier.uri | http://www.scopus.com/inward/record.url?eid=2-s2.0-65949124697&partnerID=MN8TOARS | - |
dc.identifier.uri | http://scholars.lib.ntu.edu.tw/handle/123456789/346264 | - |
dc.description.abstract | The ubiquitously expressed 14-3-3 proteins are involved in numerous important cellular functions. The loss of 14-3-3σ is a common event in breast cancer; however, the role of other 14-3-3s in breast cancer is unclear. Recently, we found that 14-3-3ζ, overexpression occurs in early stage breast diseases and contributes to transformation of human mammary epithelial cells. Here, we show that 14-3-3ζ overexpression also persisted in invasive ductal carcinoma and contributed to the further progression of breast cancer. To examine the clinical effect of 14-3-3ζ, overexpression in advanced stage breast cancer, we performed immunohistochemical analysis of 14-3-3ζ, expression in primary breast carcinomas. 14-3-3ζ, overexpression occurred in 42% of breast tumors and was determined to be an independent prognostic factor for reduced disease-free survival. 14-3-3ζ, overexpression combined with ErbB2 overexpression and positive lymph node status identified a subgroup of patients at high risk for developing distant metastasis. To investigate whether 14-3-3ζ, overexpression causally promotes breast cancer progression, we overexpressed 14-3-3ζ, by stable transfection or reduced 14-3-3ζ expression by siRNA in cancer cell lines. Increased 14-3-3ζ, expression enhanced anchorage-independent growth and inhibited stress-induced apoptosis, whereas downregulation of 14-3-3ζ, reduced anchorage-independent growth and sensitized cells to stress-induced apoptosis via the mitochondrial apoptotic pathway. Transient blockade of 14-3-3ζ expression by siRNA in cancer cells effectively reduced the onset and growth of tumor xenografts in vivo. Therefore, 14-3-3ζ, overexpression is a novel molecular marker for disease recurrence in breast cancer patients and may serve as an effective therapeutic target in patients whose tumors overexpress 14-3-3ζ ? 2009 American Association for Cancer Research. | - |
dc.language | en | en |
dc.relation.ispartof | Cancer Research | en_US |
dc.source | AH | - |
dc.subject.classification | [SDGs]SDG3 | - |
dc.subject.other | small interfering RNA; stratifin; protein 14 3 3; tumor marker; anchorage independent growth; apoptosis; article; breast cancer; cancer growth; cancer recurrence; cancer risk; cell survival; controlled study; disease free survival; down regulation; human; human cell; intraductal carcinoma; priority journal; prognosis; protein expression; tumor xenograft; biosynthesis; breast tumor; cell adhesion; cell growth; cell survival; female; gene amplification; genetics; metabolism; mitochondrion; pathology; physiology; risk factor; tumor cell line; tumor recurrence; 14-3-3 Proteins; Apoptosis; Breast Neoplasms; Cell Adhesion; Cell Growth Processes; Cell Line, Tumor; Cell Survival; Female; Gene Amplification; Humans; Mitochondria; Neoplasm Recurrence, Local; Prognosis; Risk Factors; Tumor Markers, Biological | - |
dc.title | 14-3-3ζ overexpression defines high risk for breast cancer recurrence and promotes cancer cell survival | - |
dc.type | journal article | en |
dc.identifier.doi | 10.1158/0008-5472.CAN-08-2765 | - |
dc.relation.pages | 3425-3432 | - |
dc.relation.journalvolume | 69 | - |
dc.relation.journalissue | 8 | - |
item.fulltext | no fulltext | - |
item.grantfulltext | none | - |
item.openairetype | journal article | - |
item.openairecristype | http://purl.org/coar/resource_type/c_6501 | - |
item.cerifentitytype | Publications | - |
crisitem.author.dept | Oncology-NTUH | - |
crisitem.author.orcid | 0000-0002-1575-5620 | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
顯示於: | 腫瘤醫學研究所 |
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