Regulation of PBX3 expression by androgen and Let-7d in prostate cancer

Molecular Cancer

Research

Aud Svindland¹  Viktor Berge²  Ayham Alshbib³  Kristin Austlid Taskén³  Håkon Ramberg³ 

[1] Faculty Division Aker University Hospital, University of Oslo, Department of Pathology, Oslo University Hospital, Aker, N-0514, Oslo, Norway;Faculty Division Aker University Hospital, University of Oslo, Oslo Urological University Clinic, Oslo University Hospital, Aker, N-0514, Oslo, Norway;Faculty Division Aker University Hospital, University of Oslo, Oslo Urological University Clinic, Oslo University Hospital, Aker, N-0514, Oslo, Norway;Department of Tumor Biology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway;

关键词: Prostate Cancer;    Androgen;    Androgen Receptor;    LNCaP Cell;    Prostate Cancer Cell Line;   

DOI  :  10.1186/1476-4598-10-50

 received in 2010-10-06, accepted in 2011-05-06,  发布年份 2011

来源: Springer

【 摘 要 】

BackgroundThe pre-leukemia transcription factor 3 (PBX) is part of the PBX family of transcription factors, which is known to regulate genes involved in differentiation of urogenital organs and steroidogenesis. This is of interest with regard to prostate cancer progression as regulation of steroidogenesis is one of the mechanisms involved in the development of castration-resistant prostate cancer. In light of this we wanted to investigate the possible involvement of androgen regulation of PBX3 expression in prostate cancer.ResultsIn this study, we show that PBX3 is post-transcriptionally regulated by androgen in prostate cancer cells and that the effect might be independent of the androgen receptor. Furthermore, PBX3 was identified as a target of Let-7d, an androgen regulated microRNA. Let-7d was down-regulated in malignant compared to benign prostate tissue, whereas up-regulation of PBX3 expression was observed.ConclusionsWe demonstrate that PBX3 is up-regulated in prostate cancer and post- transcriptionally regulated by androgen through Let-7d.

【 授权许可】

Unknown   
© Ramberg et al; licensee BioMed Central Ltd. 2011. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.