Upregulation of SATB1 is associated with prostate cancer aggressiveness and disease progression.
Upregulation of SATB1 is associated with prostate cancer aggressiveness and disease progression.
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DOI：
10.1371/journal.pone.0053527
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Gupta S
中科院分区：
文献类型：
--
作者：
Shukla S;Sharma H;Abbas A;MacLennan GT;Fu P;Danielpour D;Gupta S
疾病侵袭性仍然是前列腺癌进展的关键因素。上皮细胞向间充质细胞系的转化，与e -钙粘蛋白的缺失相关，提供了显著的侵袭潜力和迁移能力。最近，特殊AT-rich结合蛋白（SATB1）与肿瘤进展有关。SATB1是一种细胞型限制性核蛋白，在细胞分化过程中起组织特异性DNA序列组织者的作用。我们的研究结果表明，SATB1在前列腺肿瘤的侵袭和迁移中发挥重要作用，其核定位与疾病侵袭性相关。临床标本分析显示，与低级别肿瘤和良性组织相比，SATB1主要表达于高级别肿瘤的细胞核中。与良性标本相比，在癌组织中观察到SATB1核水平的逐渐增加。同样，与非致瘤性PZ-HPV-7细胞相比，许多前列腺癌细胞（即HPV-CA-10、DU145、DUPro、PC-3、PC-3M、LNCaP和C4-2B）中SATB1蛋白水平较高。SATB1的核表达在前列腺癌细胞及其亲本细胞系的生物侵袭性亚克隆中较高。此外，异位SATB1转染增加了永活的人前列腺上皮PZ-HPV-7细胞的细胞运动性和侵袭性，这与E-cadherin表达的丧失有关。因此，在高侵袭性人前列腺癌PC-3M细胞中，敲低SATB1可抑制体内侵袭性和肿瘤生长，同时E-cadherin蛋白表达增加。我们的研究结果表明，SATB1能够通过上皮-间质转化促进前列腺癌的侵袭性。
Disease aggressiveness remains a critical factor to the progression of prostate cancer. Transformation of epithelial cells to mesenchymal lineage, associated with the loss of E-cadherin, offers significant invasive potential and migration capability. Recently, Special AT-rich binding protein (SATB1) has been linked to tumor progression. SATB1 is a cell-type restricted nuclear protein, which functions as a tissue-specific organizer of DNA sequences during cellular differentiation. Our results demonstrate that SATB1 plays significant role in prostate tumor invasion and migration and its nuclear localization correlates with disease aggressiveness. Clinical specimen analysis showed that SATB1 was predominantly expressed in the nucleus of high-grade tumors compared to low-grade tumor and benign tissue. A progressive increase in the nuclear levels of SATB1 was observed in cancer tissues compared to benign specimens. Similarly, SATB1 protein levels were higher in a number of prostate cancer cells viz. HPV-CA-10, DU145, DUPro, PC-3, PC-3M, LNCaP and C4-2B, compared to non-tumorigenic PZ-HPV-7 cells. Nuclear expression of SATB1 was higher in biologically aggressive subclones of prostate cancer cells with their respective parental cell lines. Furthermore, ectopic SATB1 transfection conferred increased cell motility and invasiveness in immortalized human prostate epithelial PZ-HPV-7 cells which correlated with the loss of E-cadherin expression. Consequently, knockdown of SATB1 in highly aggressive human prostate cancer PC-3M cells inhibited invasiveness and tumor growth in vivo along with increase in E-cadherin protein expression. Our findings demonstrate that SATB1 has ability to promote prostate cancer aggressiveness through epithelial-mesenchymal transition.
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影响因子：
14.9
作者：
Gong F;Sun L;Wang Z;Shi J;Li W;Wang S;Han X;Sun Y
通讯作者：
Sun Y
影响因子：
12.4
作者：
Li, Q-Q;Chen, Z-Q;Xu, Z-D
通讯作者：
Xu, Z-D
SATB1是中国人群胃癌的独立预后标志物
影响因子：
4.2
作者：
Lu, Xiaoming;Cheng, Chao;Tong, Qiang
通讯作者：
Tong, Qiang
影响因子：
6.6
作者：
GINGRICH, JR;TUCKER, JA;WEBB, KS
通讯作者：
WEBB, KS
影响因子：
4.4
作者：
Szemes, M;Gyorgy, A;Agoston, DV
通讯作者：
Agoston, DV