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Published in: Journal of Translational Medicine 1/2013

Open Access 01-12-2013 | Research

SATB1 is overexpressed in metastatic prostate cancer and promotes prostate cancer cell growth and invasion

Authors: Lijun Mao, Chunhua Yang, Junqi Wang, Wang Li, Rumin Wen, Jiacun Chen, Junnian Zheng

Published in: Journal of Translational Medicine | Issue 1/2013

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Abstract

Background

Special AT-rich sequence binding protein 1 (SATB1) is a nuclear factor that functions as the global chromatin organizer to regulate chromatin structure and gene expression gene expression. SATB1 has been shown to be abnormally expressed in various types of cancer. However, the expression and role of SATB1 in prostate cancer remain unclear.

Methods

120 cases of prostatic carcinoma and 60 cases of benign prostate hyperplasia were analyzed for SATB1 expression by immunohistochemistry. LNCaP, DU-145, and PC3 prostate cancer cells were examined for SATB1 expression by Western blot analysis. Cell proliferation and invasion was evaluated by CCK8 and transwell invasion assay, respectively.

Results

SATB1 staining was stronger in prostatic carcinomas with metastasis than in those without metastasis, but was absent in benign prostate hyperplasia. Furthermore, SATB1 expression was positively correlated with bone metastasis and the Gleason score. SATB1 overexpression promoted the proliferation and invasion of LNCaP cells while SATB1 knockdown inhibited the proliferation and invasion of DU-145 cells.

Conclusions

These findings provide novel insight into oncogenic role of SATB1 in prostate cancer, suggesting that SATB1 is a promising biomarker and therapeutic target for prostate cancer.
Appendix
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Metadata
Title
SATB1 is overexpressed in metastatic prostate cancer and promotes prostate cancer cell growth and invasion
Authors
Lijun Mao
Chunhua Yang
Junqi Wang
Wang Li
Rumin Wen
Jiacun Chen
Junnian Zheng
Publication date
01-12-2013
Publisher
BioMed Central
Published in
Journal of Translational Medicine / Issue 1/2013
Electronic ISSN: 1479-5876
DOI
https://doi.org/10.1186/1479-5876-11-111

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