Chia Nan University of Pharmacy & Science Institutional Repository:Item 310902800/28677
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 18034/20233 (89%)
Visitors : 23365686      Online Users : 494
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
  • Adv. Search
    HomeLoginUploadHelpAboutAdminister Goto mobile version
    Please use this identifier to cite or link to this item: https://ir.cnu.edu.tw/handle/310902800/28677


    Title: RHBDL2 Is a Critical Membrane Protease for Anoikis Resistance in Human Malignant Epithelial Cells
    Authors: Cheng, Tsung-Lin
    Lai, Chao-Han
    Jiang, Shinn-Jong
    Hung, Jui-Hsiang
    Liu, Shi-Kai
    Chang, Bi-Ing
    Shi, Guey-Yueh
    Wu, Hua-Lin
    Contributors: 生物科技系
    Keywords: RHOMBOID PROTEASE
    CANCER-CELLS
    APOPTOSIS
    DROSOPHILA
    ACTIVATION
    THROMBOMODULIN
    INTEGRINS
    ADHESION
    MATRIX
    GENE
    Date: 2014
    Issue Date: 2015-05-06 21:24:49 (UTC+8)
    Publisher: Hindawi Publishing Corporation
    Abstract: Anoikis resistance allows metastatic tumor cells to survive in a homeless environment. Activation of epithelial growth factor receptor (EGFR) signaling is one of the key mechanisms for metastatic tumor cells to resist anoikis, yet the regulation mechanisms of homeless-triggered EGFR activation in metastatic tumor cells remain unclear. Rhomboid-like-2 (RHBDL2), an evolutionally conserved intramembrane serine protease, can cleave the EGF ligand and thus trigger EGFR activation. Herein, we demonstrated that RHBDL2 overexpression in human epithelial cells resulted in promotion of cell proliferation, reduction of cell adhesion, and suppression of anoikis. During long-term suspension cultures, increased RHBDL2 was only detected in aggressive tumor cell lines. Treatment with the rhomboid protease inhibitor or RHBDL2 shRNA increased cleaved caspase 3, a marker of apoptosis. Finally, inhibition of EGFR activation increased the cleaved caspase 3 and attenuated the detachment-induced focal adhesion kinase phosphorylation. Taken together, these findings provide evidence for the first time that RHBDL2 is a critical molecule in anoikis resistance of malignant epithelial cells, possibly through the EGFR-mediated signaling. Our study demonstrates RHBDL2 as a new therapeutic target for cancer metastasis.
    Relation: Scientific World Journal, 90287
    Appears in Collections:[Dept. of Biotechnology (including master's program)] Periodical Articles

    Files in This Item:

    File Description SizeFormat
    index.html0KbHTML1432View/Open


    All items in CNU IR are protected by copyright, with all rights reserved.


    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - Feedback