Elevated expression of SATB1 is involved in pancreatic tumorigenesis and is associated with poor patient survival.

Abstract

Special AT-rich sequence-binding protein 1 (SATB1) is a master chromatin organizer which has been reported to be implicated in tumor progression in breast and lung cancer. However, its functions in pancreatic tumorigenesis have yet to be elucidated. In the present study, the involvement of SATB1 in pancreatic cancer development was investigated in human BxPC-3 pancreatic adenocarcinoma cells. Short hairpin (sh)RNA was used to stably downregulate SATB1 expression, and functional assays, including cell proliferation, colony formation, soft agar and migration assays, were performed in vitro. In addition, a mouse pancreatic cancer xenograft model was created to examine the tumor-promoting properties of SATB1 in vivo. The present findings demonstrated that stable knockdown of SATB1 expression inhibited the proliferation, colony formation, anchorage-independent growth and suppressed the migratory capabilities of BxPC-3 cells in vitro. In addition, SATB1 downregulation significantly inhibited tumor growth in xenografted mice in vivo. Furthermore, SATB1 was revealed to be upregulated in human pancreatic cancer tissue samples compared with matched non-cancerous adjacent tissues, and high SATB1 expression was associated with poor patient survival. Overall, the present study demonstrated that SATB1 promoted the proliferation of pancreatic cancer cells in vitro. In addition, SATB1 expression was revealed to be upregulated in human pancreatic cancer tissues and its upregulation was associated with poor patient survival. Therefore, SATB1 may have potential as a novel prognostic biomarker and therapeutic target for the treatment of patients with pancreatic cancer.