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  1. NTU Scholars
  2. 醫學院
  3. 醫學院附設醫院 (臺大醫院)
Please use this identifier to cite or link to this item: https://scholars.lib.ntu.edu.tw/handle/123456789/551205
Title: Bortezomib suppresses focal adhesion kinase expression via interrupting nuclear factor-kappa B
Authors: BOR-SHENG KO 
Chang T.-C.
Chen C.-H.
Liu C.-C.
Kuo C.-C.
CHIUN HSU 
Ying-Chun Shen 
Shen T.-L.
Golubovskaya V.M.
Chang C.-C.
Shyue S.-K.
Liou J.-Y.
Issue Date: 2010
Journal Volume: 86
Journal Issue: 5��6��
Start page/Pages: 199-206
Source: Life Sciences
Abstract: 
Aims: Bortezomib is a potent proteasome inhibitor currently used to treat various malignancies with promising results. To explore the role of bortezomib in reducing cancer cell migration and inducing apoptosis, we evaluated the effects of bortezomib on the expression of focal adhesion kinase (FAK). Main methods: Various types of cancer cells including lung cancer A549, H1299; a breast cancer MCF7; a hepatocellular carcinoma Huh7, and a tongue squamous cell carcinoma SCC-25 were treated with different concentrations of bortezomib or MG-132 as indicated for 24. h. Protein and mRNA levels were determined by Western blotting and real-time PCR. Apoptosis was analyzed by caspase 3 cleavage and activity. FAK promoter and NFκB binding activities were measured by luciferase-reporter method. NFκB subunit p65 binding capacity was determined by electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) analysis. Key findings: Both bortezomib and another proteasome inhibitor, MG-132, significantly reduced FAK expression, suppressed cancer cell migration and increased cell apoptosis. Results of real-time PCR and promoter activity assay revealed that bortezomib decreased FAK expression through transcriptional inactivation. Results of FAK promoter activity and ChIP assays in A549 and H1299 cells indicated that bortezomib suppressed FAK activity through a p53-independent pathway. Furthermore, reduction of NFκB binding capacity demonstrated by EMSA and ChIP assay suggested that NFκB plays an important role in bortezomib suppressing FAK expression. Significance: These results suggested that FAK is downregulated by bortezomib through a proteasome-dependent NFκB inhibitory mechanism. Thus, FAK could be a potential molecular target of bortezomib for therapeutic strategy. ? 2009 Elsevier Inc.
URI: https://www.scopus.com/inward/record.uri?eid=2-s2.0-74749103461&doi=10.1016%2fj.lfs.2009.12.003&partnerID=40&md5=b2829ed4a9a9b15fa49449904d7151eb
https://scholars.lib.ntu.edu.tw/handle/123456789/551205
ISSN: 0024-3205
DOI: 10.1016/j.lfs.2009.12.003
SDG/Keyword: benzyloxycarbonylleucylleucylleucinal; bortezomib; caspase 3; focal adhesion kinase; immunoglobulin enhancer binding protein; transcription factor RelA; apoptosis; article; cancer cell; concentration response; controlled study; down regulation; drug targeting; gene expression; gene repression; human; human cell; migration inhibition; protein expression; transcription regulation; Antineoplastic Agents; Apoptosis; Blotting, Western; Boronic Acids; Cell Line, Tumor; Cell Movement; Down-Regulation; Electrophoretic Mobility Shift Assay; Enzyme Inhibitors; Focal Adhesion Protein-Tyrosine Kinases; Humans; In Situ Nick-End Labeling; NF-kappa B; Proteasome Endopeptidase Complex; Pyrazines; Reverse Transcriptase Polymerase Chain Reaction
[SDGs]SDG3
Appears in Collections:醫學院附設醫院 (臺大醫院)

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臺大位居世界頂尖大學之列,為永久珍藏及向國際展現本校豐碩的研究成果及學術能量,圖書館整合機構典藏(NTUR)與學術庫(AH)不同功能平台,成為臺大學術典藏NTU scholars。期能整合研究能量、促進交流合作、保存學術產出、推廣研究成果。

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