RUNX2 is overexpressed in melanoma cells and mediates their migration and invasion

被引：33
|
作者：
Boregowda, Rajeev K. [1 ]
Olabisi, Oyenike O. [1 ]
Abushahba, Walid [1 ]
Jeong, Byeong-Seon [2 ]
Haenssen, Keneshia K. [2 ]
Chen, Wenjin [3 ]
Chekmareva, Marina [4 ]
Lasfar, Ahmed [5 ]
Foran, David J. [3 ]
Goydos, James S. [2 ]
Cohen-Solal, Karine A. [1 ]
机构：
[1] Rutgers State Univ, Robert Wood Johnson Med Sch, Rutgers Canc Inst New Jersey, Dept Med,Div Med Oncol, New Brunswick, NJ 08903 USA
[2] Rutgers State Univ, Robert Wood Johnson Med Sch, Rutgers Canc Inst New Jersey, Dept Surg,Div Surg Oncol, New Brunswick, NJ 08903 USA
[3] Rutgers Canc Inst New Jersey, Ctr Biomed Imaging & Informat, New Brunswick, NJ 08903 USA
[4] Robert Wood Johnson Univ Hosp, Dept Pathol & Lab Med, Rutgers Canc Inst New Jersey, New Brunswick, NJ 08901 USA
[5] Rutgers State Univ, Dept Pharmacol & Toxicol, Ernest Mario Sch Pharm, Piscataway, NJ 08854 USA
来源：
CANCER LETTERS | 2014年 / 348卷 / 1-2期
关键词：
Melanoma; Transcription factor; RUNX2; FAR; Migration; Cholecalciferol (Vitamin D3); FOCAL ADHESION KINASE; MALIGNANT-MELANOMA; GENE-EXPRESSION; METASTATIC MELANOMA; BRAF MUTATIONS; CANCER; PROLIFERATION; SENESCENCE; DIFFERENTIATION; ACTIVATION;
D O I：
10.1016/j.canlet.2014.03.011
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
In the present study, we investigated the role of the transcription factor RUNX2 in melanomagenesis. We demonstrated that the expression of transcriptionally active RUNX2 was increased in melanoma cell lines as compared with human melanocytes. Using a melanoma tissue microarray, we showed that RUNX2 levels were higher in melanoma cells as compared with nevic melanocytes. RUNX2 knockdown in melanoma cell lines significantly decreased Focal Adhesion Kinase expression, and inhibited their cell growth, migration and invasion ability. Finally, the pro-hormone cholecalciferol reduced RUNX2 transcriptional activity and decreased migration of melanoma cells, further suggesting a role of RUNX2 in melanoma cell migration. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码：61 / 70
页数：10
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