Format

Send to

Choose Destination
Nat Rev Urol. 2017 Jan;14(1):38-48. doi: 10.1038/nrurol.2016.225. Epub 2016 Nov 22.

The role of GATA2 in lethal prostate cancer aggressiveness.

Author information

1
Department of Pathology, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA.
2
Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA.
3
Department of Hematology and Oncology, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA.

Abstract

Advanced prostate cancer is a classic example of the intractability and consequent lethality that characterizes metastatic carcinomas. Novel treatments have improved the survival of men with prostate cancer; however, advanced prostate cancer invariably becomes resistant to these therapies and ultimately progresses to a lethal metastatic stage. Consequently, detailed knowledge of the molecular mechanisms that control prostate cancer cell survival and progression towards this lethal stage of disease will benefit the development of new therapeutics. The transcription factor endothelial transcription factor GATA-2 (GATA2) has been reported to have a key role in driving prostate cancer aggressiveness. In addition to being a pioneer transcription factor that increases androgen receptor (AR) binding and activity, GATA2 regulates a core subset of clinically relevant genes in an AR-independent manner. Functionally, GATA2 overexpression in prostate cancer increases cellular motility and invasiveness, proliferation, tumorigenicity, and resistance to standard therapies. Thus, GATA2 has a multifaceted function in prostate cancer aggressiveness and is a highly attractive target in the development of novel treatments against lethal prostate cancer.

PMID:
27872477
PMCID:
PMC5489122
DOI:
10.1038/nrurol.2016.225
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center