SATB1 promotes prostate cancer metastasis by the regulation of epithelial–mesenchymal transition

• Published in: Biomedicine & pharmacotherapy Vol. 79; pp. 1 - 8
• Main Authors: Mao, Li-jun, Yang, Chun-hua, Fan, Li, Gao, Peng, Yang, Dong-rong, Xue, Bo-xin, Zheng, Jun-nian, Shan, Yu-xi
• Format: Journal Article
• Language: English
• Published: France Elsevier Masson SAS 01.04.2016
• Subjects: Animals; Biomarkers, Tumor - metabolism; Cadherins - metabolism; Cell Line, Tumor; Cell Proliferation; Epithelial-Mesenchymal Transition; Gene Expression Regulation, Neoplastic; Gene Silencing; Internal Medicine; Invasion; Male; Matrix Attachment Region Binding Proteins - genetics; Matrix Attachment Region Binding Proteins - metabolism; Matrix Metalloproteinase 2 - metabolism; Medical Education; Metastasis; Mice, Inbred BALB C; Mice, Nude; Neoplasm Metastasis; Proliferation; Prostate cancer; Prostatic Neoplasms - genetics; Prostatic Neoplasms - metabolism; Prostatic Neoplasms - pathology; SATB1; Subcutaneous Tissue - pathology; Vimentin - metabolism; Xenograft Model Antitumor Assays; Metastasis; Proliferation; SATB1; Prostate cancer; Invasion
• ISSN: 0753-3322; 1950-6007
• DOI: 10.1016/j.biopha.2016.01.038

Abstract Special AT-rich sequence binding protein 1 (SATB1) plays important role in the regulation of chromatin structure and gene expression. Recent studies have indicated oncogenic role of SATB1. However, the function of SATB1 in prostate cancer progression and metastasis remains unclear. In this study SATB1 expression vector or siRNA was employed to modulate the expression level of SATB1 in prostate cancer cells and xenograft tumor in nude mouse model. Immunohistochemical analysis was performed on clinical prostate cancer samples. Silencing SATB1 inhibited the growth of DU-145 cells subcutaneous tumor in nude mice, while SATB1 overexpression promoted the growth of LNCaP cells subcutaneous tumor in nude mice. Immunohistochemical and Western blot analysis of the xenografts showed that silencing SATB1 led to decreased expression of vimentin and MMP2 and increased expression of E-cadherin, while SATB1 overexpression led to increased expression of vimentin and MMP2 and decreased expression of E-cadherin. Furthermore, SATB1, vimentin and MMP2 expression was increased significantly while E-cadherin expression was reduced significantly in clinical samples of prostate carcinoma with metastasis compared to prostate carcinoma without metastasis and benign prostate hyperplasia. Taken together, these findings suggest that the modulation of epithelial–mesenchymal transition by SATB1 may contribute to prostate cancer metastasis.