AT-rich sequence binding protein 1: Contribution to tumor progression and metastasis of human ovarian carcinoma

Special AT-rich sequence binding protein 1 (SATB1) is a master chromatin organizer that has recently been reported to directly upregulate metastasis-associated genes and downregulate tumor suppressor genes. However, its clinical significance in the case of ovarian cancer remains unclear. In the current study, we assessed the expression levels of SATB1 in ovarian cancer and aimed to show whether it may be a conventional clinicopathological parameter. Epithelial ovarian cancer (n=91), borderline cystadenoma (n=13) and normal ovarian background tissues (n=8) were collected immediately following excision during surgery. The mRNA expression levels of SATB1, VEGF-A and MMP-9 were determined using real-time quantitative PCR. Western blotting and immunohistochemical staining were carried out to detect the protein expression levels of SATB1. Expression levels within the ovarian cancer specimens were compared to the normal background tissues and analyzed against FIGO stage, lymph node involvement and histological type. SATB1 mRNA in malignant and borderline ovarian cystadenoma tissues was 6.74- and 5.70-fold higher compared with normal ovarian tissue, respectively (P<0.01). Western blot analysis revealed that a strong positive band of SATB1 expression was present in ovarian cancer tissues. Immunohistochemical staining showed that the positive expression rates of SATB1 in ovarian cancer, borderline ovarian cystadenoma and normal ovarian tissues were 69.2, 61.5 and 0% (P<0.01), respectively. SATB1 expression increased concomitantly with increasing FIGO stage and lymph node involvement. Survival curves showed that a higher SATB1 expression was correlated with shorter survival. Our results provide evidence that SATB1 expression is significantly associated with progression, metastasis and prognosis of epithelial ovarian cancer. SATB1 may therefore serve as a conventional clinicopathological parameter of ovarian cancer.