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BACKGROUND Pancreatic cancer is one of the most aggressive and lethal malignancies and it is the eighth most common cause of death from cancer worldwide. The purpose of this study was to investigate the role of GSG2 (HASPIN) in the development and progression of pancreatic cancer. MATERIAL AND METHODS GSG2 expression was detected by immunohistochemistry in tumor tissue samples, and by qRT-PCR and Western blot assay in human pancreatic cancer cell lines. Cell proliferation was evaluated by MTT assay. Giemsa staining was used for analyzing colony formation. Cell cycle and cell apoptosis were determined using Fluorescence activated Cells Sorting. Wound healing assay and transwell assay were applied for examining cell migration. The molecular mechanism was investigated by human apoptosis antibody array. Tumor-bearing animal model was constructed to verify the effects of GSG2 on pancreatic cancer in vivo. RESULTS GSG2 expression was upregulated in pancreatic cancer tissues and human pancreatic cancer cell lines: PANC-1 and SW1990. Higher expression of GSG2 in tumor samples was associated with poorer prognosis. GSG2 knockdown suppressed cell proliferation, colony formation, metastasis and promoted cell apoptosis, which was also verified in vivo. In addition, GSG2 knockdown blocked the cell cycle in G2. It was also found that downregulation of GSG2 inhibited Bcl-2, Bcl-w, cIAP, HSP60 and Livin expression as well as promoted IGFBP-6 expression. CONCLUSION This study revealed that GSG2 upregulation was associated with pancreatic cancer progression. GSG2 knockdown inhibited cell proliferation, colony formation and migration, blocked cell cycle at G2 phase, and induced cell apoptosis. Therefore, GSG2 might serve as a potential therapeutic target for pancreatic cancer therapy and a market for prognosis.