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| 題名: | Akt3 controls vascular endothelial growth factor secretion and angiogenesis in ovarian cancer cells |
| 作者: | 徐沺;Liby, Tiera A.;Spyropoulos, Perry;Buff Lindner, Haley;Eldridge, Juanita;Beeson, Craig;Hsu, Tien;Muise-Helmericks, Robin C. |
| 貢獻者: | 生醫理工學院生醫科學與工程學系 |
| 關鍵詞: | Animals;Antigens, Neoplasm - metabolism;Biological and medical sciences;Biomarkers, Tumor - metabolism;Cancer;Cell Line, Tumor;Endoplasmic Reticulum - metabolism;Female;Female genital diseases;Gene expression;Gene Expression Regulation, Neoplastic;Gene Silencing;Gynecology. Andrology. Obstetrics;Humans;Kinases;Medical research;Medical sciences;Mice;Mice, SCID;Mitochondria - genetics;Mitochondria - metabolism;Neovascularization, Pathologic - genetics;Ovarian cancer;Ovarian Neoplasms - blood supply;Ovarian Neoplasms - enzymology;Ovarian Neoplasms - genetics;Proto-Oncogene Proteins c-akt - genetics;Proto-Oncogene Proteins c-akt - metabolism;PTEN Phosphohydrolase - metabolism;Signal Transduction;Tumor Burden - genetics;Tumors;Vascular endothelial growth factor;Vascular Endothelial Growth Factor A - metabolism;Xenograft Model Antitumor Assays |
| 日期: | 2012-02-01 |
| 上傳時間: | 2026-04-23 11:14:59 (UTC+8) |
| 出版者: | Wiley-Liss Inc.;Hoboken: Wiley Subscription Services, Inc., A Wiley Company |
| 摘要: | 摘要： AbstractThe PI3 kinase/Akt pathway is commonly deregulated in human cancers, functioning in such processes as proliferation, glucose metabolism, survival and motility. We have previously described a novel function for one of the Akt isoforms (Akt3) in primary endothelial cells: the control of VEGF‐induced mitochondrial biogenesis. We sought to determine if Akt3 played a similar role in carcinoma cells. Because the PI3 kinase/Akt pathway has been strongly implicated as a key regulator in ovarian carcinoma, we tested the role of Akt3 in this tumor type. Silencing of Akt3 by shRNA did not cause an overt reduction in mitochondrial gene expression in a series of PTEN positive ovarian cancer cells. Rather, we find that blockade of Akt3, results in smaller, less vascularized tumors in a xenograft mouse model that is correlated with a reduction in VEGF expression. We find that blockade of Akt3, but not Akt1, results in a reduction in VEGF secretion and retention of VEGF protein in the endoplasmic reticulum (ER). The reduction in secretion under conditions of Akt3 blockade is, at least in part, due to the down regulation of the resident golgi protein and reported tumor cell marker, RCAS1. Conversely, over‐expression of Akt3 results in an increase in RCAS1 expression and in VEGF secretion. Silencing of RCAS1 using siRNA inhibits VEGF secretion. These findings suggest an important role for Akt3 in the regulation of RCAS1 and VEGF secretion in ovarian cancer cells.
其他題名： Int. J. Cancer
出版者： Hoboken: Wiley Subscription Services, Inc., A Wiley Company
出版日期： 2012-02-01
出處： International Journal of Cancer, 2012-02, Vol.130 (3), p.532-543
資源來源： Wiley Online Library
版權： Copyright © 2011 UICC
版權： 2015 INIST-CNRS
版權： Copyright © 2011 UICC.
識別號： ISSN: 0020-7136
識別號： ISSN: 1097-0215
識別號： EISSN: 1097-0215
識別號： DOI: 10.1002/ijc.26010
識別號： PMID: 21351097
識別號： CODEN: IJCNAW |
| 顯示於類別: | [生醫科學與工程學系] 期刊論文
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