ASIA unversity:Item 310904400/86865
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    Title: 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
    Authors: Su, Ying-Fang;Su, Ying-Fang;Lian, Chi-Yen;Liang, Chi-Yen;黃志揚;Huang, Chih-yang;Peng, Chih-Yu;Peng, Chih-Yu;Chiyu, Claire;Chen, Claire Chiyu;Ming-Cheng, L;Lin, Ming-Cheng;Lin, Rong-Kai;Lin, Rong-Kai;Lin, Wei-Wen;Lin, Wei-Wen;Lia, Pao-Hsin;Liao, Pao-Hsin;Yang, Jaw-Ji;Yang, Jaw-Ji;*
    Contributors: 生物科技學系
    Keywords: Anchorage-independent growth;Oral cancer;Extracellular-signal-regulated kinases;Rac1;DEPDC1B
    Date: 2014
    Issue Date: 2014-11-07 14:43:44 (UTC+8)
    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.
    Relation: JOURNAL OF BIOMEDICAL SCIENCE
    Appears in Collections:[Department of Biotechnology] Journal Article

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