DAB2IP in cancer
Abstract
// Liang Liu 1, 2, * , Cong Xu 3, * , Jer-Tsong Hsieh 4 , Jianping Gong 1, 2 , Daxing Xie 1, 2 1 Tongji Cancer Research Institute, Tongji Hospital, Tongji Medical College in Huazhong University of Science and Technology, Wuhan, Hubei 430030, China 2 Department of Gastrointestinal Surgery, Tongji Hospital, Tongji Medical College in Huazhong University of Science and Technology, Wuhan, Hubei 430030, China 3 Department of Gastroenterology, Tongji Hospital, Tongji Medical College in Huazhong University of Science and Technology, Wuhan, Hubei 430030, China 4 Department of Urology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA * These authors contributed equally to this work Correspondence to: Daxing Xie, e-mail: dxxie@tjh.tjmu.edu.cn Jianping Gong, e-mail: jpgong@tjh.tjmu.edu.cn Jer-Tsong Hsieh, e-mail: jt.hsieh@utsouthwestern.edu Keywords: DAB2IP, AIP1, cancer, tumor suppressor Received: July 23, 2015 Accepted: November 15, 2015 Published: December 08, 2015 ABSTRACT 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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