Knockdown of GSG2 Suppresses the Progression of Colorectal Cancer Cells.

Abstract

Introduction: As a serine/threonine kinase, Haspin (GSG2) has been reportedly associated with the development of malignant tumors. However, few studies have reported the role of GSG2 in colorectal cancer (CRC). Materials and Methods: Based on data from the Oncomine databases, GSG2 was found to be highly expressed in CRC patients' tissues. Therefore, the expression of GSG2 in CRC cell lines was subsequently evaluated. GSG2 loss-of-function experiments were conducted by infection with a lentivirus expressing shRNAs against GSG2. Colony-formation and cell viabilities were assessed using clonogenic and 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays, respectively. Migration was assessed using wound-healing and transwell assays. A GSG2 inhibitor experiment was used to investigate the key role of GSG2 in CRC. Immunoprecipitation was used to investigate the interaction between GSG2 and p-H3. In addition, apoptosis was evaluated by quantifying caspase 3/7 activities, and western blot analyses were used to investigate the underlying mechanisms of GSG2 in CRC. Results: GSG2 was found to be highly expressed in CRC tissues and cells. Furthermore, GSG2 knock-down suppressed proliferation, colony formation and invasion, and induced apoptosis in CRC cells. Mechanistically, GSG2 was revealed to regulate Myc, NF-κB, Snail-1, and β-catenin signaling. Conclusion: Collectively, we demonstrate that GSG2 is a potential biomarker of CRC, and that GSG2 interference suppresses the progression of CRC and promotes apoptosis in vitro. These data suggest GSG2 as a putative oncogene, but will require additional in vivo studies to confirm.