中山醫學大學機構典藏 CSMUIR:Item 310902500/10557
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    题名: A putative novel protein, DEPDC1B, is overexpressed in oral cancer patients, and enhanced anchorage-independent growth in oral cancer cells that is mediated by Rac1 and ERK.
    作者: Su, Ying-Fang
    Liang, Chi-Yen
    Huang, Chih-Yang
    Peng, Chih-Yu
    Chen, Claire Chiyu
    Lin, Ming-Cheng
    Lin, Rong-Kai
    Lin, Wei-Wen
    Chou, Ming-Yung
    Liao, Pao-Hsin
    Jaw-Ji Yang
    贡献者: 中山醫學大學
    关键词: : Anchorage-independent growth, Oral cancer, Extracellular-signal-regulated kinases, Rac1, DEPDC1B
    日期: 2014
    上传时间: 2015-03-27T08:24:07Z (UTC)
    ISSN: 1021-7770
    摘要: Abstract
    Background: The DEP domain is a globular domain containing approximately 90 amino acids, which was first
    discovered in 3 proteins: Drosophila disheveled, Caenorhabditis elegans EGL-10, and mammalian Pleckstrin; hence
    the term, DEP. DEPDC1B is categorized as a potential Rho GTPase-activating protein. The function of the DEP
    domain in signal transduction pathways is not fully understood. The DEPDC1B protein exhibits the characteristic
    features of a signaling protein, and contains 2 conserved domains (DEP and RhoGAP) that are involved in Rho
    GTPase signaling. Small GTPases, such as Rac, CDC42, and Rho, regulate a multitude of cell events, including cell
    motility, growth, differentiation, cytoskeletal reorganization and cell cycle progression.
    Results: In this study, we found that it was a guanine nucleotide exchange factor and induced both cell migration
    in a cultured embryonic fibroblast cell line and cell invasion in cancer cell lines; moreover, it was observed to
    promote anchorage-independent growth in oral cancer cells. We also demonstrated that DEPDC1B plays a role
    in regulating Rac1 translocated onto cell membranes, suggesting that DEPDC1B exerts a biological function by
    regulating Rac1. We examined oral cancer tissue; 6 out of 7 oral cancer tissue test samples overexpressed DEPDC1B
    proteins, compared with normal adjacent tissue.
    Conclusions: DEPDC1B was a guanine nucleotide exchange factor and induced both cell migration in a cultured
    embryonic fibroblast cell line and cell invasion in cancer cell lines; moreover, it was observed to promote
    anchorage-independent growth in oral cancer cells. We also demonstrated that DEPDC1B exerts a biological
    function by regulating Rac1. We found that oral cancer samples overexpressed DEPDC1B proteins, compared
    with normal adjacent tissue. Suggest that DEPDC1B plays a role in the development of oral cancer. We revealed that
    proliferation was linked to a novel DEPDC1B-Rac1-ERK1/2 signaling axis in oral cancer cell lines.
    URI: https://ir.csmu.edu.tw:8080/ir/handle/310902500/10557
    http://dx.doi.org/10.1186/s12929-014-0067-1
    關聯: Su et al. Journal of Biomedical Science 2014, 21:67
    显示于类别:[牙醫學系暨碩士班] 期刊論文

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