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Bladder cancer is the most commonly diagnosed malignant tumor in urological system worldwide. The relationship between GSG2 and bladder cancer has not been demonstrated and remains unclear. In this study, it was demonstrated that GSG2 was up-regulated in bladder cancer tissues compared with the normal tissues and its high expression was correlated with more advanced malignant grade and lower survival rate. Further investigations indicated that the overexpression/knockdown of GSG2 could promote/inhibit proliferation, colony formation and migration of bladder cancer cells, while inhibiting/promoting cell apoptosis. Moreover, knockdown of GSG2 could also suppress tumorigenicity of bladder cancer cells in vivo . RNA-sequencing followed by Ingenuity pathway analysis (IPA) was performed for exploring downstream of GSG2 and identified KIF15 as the potential target. Furthermore, our study revealed that knockdown of KIF15 could inhibit development of bladder cancer in vitro , and alleviate the GSG2 overexpression induced promotion of bladder cancer. In conclusion, our study showed, as the first time, GSG2 as a prognostic indicator and tumor promotor for bladder cancer, whose function was carried out probably through the regulation of KIF15.

GSG2 (Haspin) promotes development and progression of bladder cancer through targeting KIF15 (Kinase-12)