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DAB2IP in cancer

DOC-2/DAB2 is a member of the disable gene family that features tumor-inhibiting activity. The DOC-2/DAB2 interactive protein, DAB2IP, is a new member of the Ras GTPase-activating protein family. It interacts directly with DAB2 and has distinct cellular functions such as modulating different signal...

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Detalles Bibliográficos
Autores principales: Liu, Liang, Xu, Cong, Hsieh, Jer-Tsong, Gong, Jianping, Xie, Daxing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4826168/
https://www.ncbi.nlm.nih.gov/pubmed/26658103
http://dx.doi.org/10.18632/oncotarget.6501
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author Liu, Liang
Xu, Cong
Hsieh, Jer-Tsong
Gong, Jianping
Xie, Daxing
author_facet Liu, Liang
Xu, Cong
Hsieh, Jer-Tsong
Gong, Jianping
Xie, Daxing
author_sort Liu, Liang
collection PubMed
description DOC-2/DAB2 is a member of the disable gene family that features tumor-inhibiting activity. The DOC-2/DAB2 interactive protein, DAB2IP, is a new member of the Ras GTPase-activating protein family. It interacts directly with DAB2 and has distinct cellular functions such as modulating different signal cascades associated with cell proliferation, survival, apoptosis and metastasis. Recently, DAB2IP has been found significantly down regulated in multiple types of cancer. The aberrant alteration of DAB2IP in cancer is caused by a variety of mechanisms, including the aberrant promoter methylation, histone deacetylation, and others. Reduced expression of DAB2IP in neoplasm may indicate a poor prognosis of many malignant cancers. Moreover, DAB2IP stands for a promising direction for developing targeted therapies due to its capacity to inhibit tumor cell growth in vitro and in vivo. Here, we summarize the present understanding of the tumor suppressive role of DAB2IP in cancer progression; the mechanisms underlying the dysregulation of DAB2IP; the gene functional mechanism and the prospects of DAB2IP in the future cancer research.
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spelling pubmed-48261682016-05-09 DAB2IP in cancer Liu, Liang Xu, Cong Hsieh, Jer-Tsong Gong, Jianping Xie, Daxing Oncotarget Review DOC-2/DAB2 is a member of the disable gene family that features tumor-inhibiting activity. The DOC-2/DAB2 interactive protein, DAB2IP, is a new member of the Ras GTPase-activating protein family. It interacts directly with DAB2 and has distinct cellular functions such as modulating different signal cascades associated with cell proliferation, survival, apoptosis and metastasis. Recently, DAB2IP has been found significantly down regulated in multiple types of cancer. The aberrant alteration of DAB2IP in cancer is caused by a variety of mechanisms, including the aberrant promoter methylation, histone deacetylation, and others. Reduced expression of DAB2IP in neoplasm may indicate a poor prognosis of many malignant cancers. Moreover, DAB2IP stands for a promising direction for developing targeted therapies due to its capacity to inhibit tumor cell growth in vitro and in vivo. Here, we summarize the present understanding of the tumor suppressive role of DAB2IP in cancer progression; the mechanisms underlying the dysregulation of DAB2IP; the gene functional mechanism and the prospects of DAB2IP in the future cancer research. Impact Journals LLC 2015-12-08 /pmc/articles/PMC4826168/ /pubmed/26658103 http://dx.doi.org/10.18632/oncotarget.6501 Text en Copyright: © 2016 Liu et al. http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Review
Liu, Liang
Xu, Cong
Hsieh, Jer-Tsong
Gong, Jianping
Xie, Daxing
DAB2IP in cancer
title DAB2IP in cancer
title_full DAB2IP in cancer
title_fullStr DAB2IP in cancer
title_full_unstemmed DAB2IP in cancer
title_short DAB2IP in cancer
title_sort dab2ip in cancer
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4826168/
https://www.ncbi.nlm.nih.gov/pubmed/26658103
http://dx.doi.org/10.18632/oncotarget.6501
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