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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
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نویسنده
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su y.-f. ,liang c.-y. ,huang c.-y. ,peng c.-y. ,chen c.c. ,lin m.-c. ,lin r.-k. ,lin w.-w. ,chou m.-y. ,liao p.-h. ,yang j.-j.
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منبع
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journal of biomedical science - 2014 - دوره : 21 - شماره : 1
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چکیده
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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. © 2014 su et al.; licensee biomed central.
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کلیدواژه
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Anchorage-independent growth; DEPDC1B; Extracellular-signal-regulated kinases; Oral cancer; Rac1
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آدرس
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institute of medicine,school of dentistry,taichung,402,taiwan,chung-shan medical university,school of dentistry,taichung,402,taiwan,department of stomatology,chung-shan medical university hospital,taichung,402, Taiwan, chiayi christian hospital,chiayi,600, Taiwan, graduate institute of chinese medical science,graduate institute of basic medical science,taichung,404,taiwan,china medical university,taichung,404,taiwan,department of health and nutrition biotechnology,asia university,taichung,413, Taiwan, institute of medicine,school of dentistry,taichung,402, Taiwan, department of chemistry and biochemistry,university of california at los angeles,cardiovascular center,los angeles,ca 90095, United States, chung-shan medical university,school of dentistry,taichung,402, Taiwan, institute of medicine,school of dentistry,taichung,402, Taiwan, veterans general hospital,taichung,407, Taiwan, institute of medicine,school of dentistry,taichung,402, Taiwan, institute of medicine,school of dentistry,taichung,402, Taiwan, institute of medicine,school of dentistry,taichung,402, Taiwan
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Authors
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