STX2 drives colorectal cancer proliferation via upregulation of EXOSC4.

Abstract Aims To explore the biological function and mechanism of Syntaxin2 (STX2) in Colorectal cancer (CRC) proliferation. Main methods A series of gain- and loss-of-function analysis were conducted to explore the biological function of STX2 in CRC proliferation in vivo and in vitro. Western blot, Co-immunoprecipitation (Co-IP) and the functional analyses were taken to analyze the regulative role of STX2 on Exosome Complex 4 (EXOSC4) in CRC proliferation; Immunohistochemistry (IHC) and Real-time quantitative polymerase chain reaction (qPCR) were used to further verify the relationship between the expression of STX2 and EXOSC4 in human CRC samples. Key findings Our study revealed that the over-expression of STX2 promoted CRC proliferation, while knockdown of STX2 repressed CRC proliferation; STX2 promoted CRC proliferation via increasing EXOSC4 protein; There was a positive correlation between STX2 and EXOSC4 expression. Significance The current data verify that STX2 drives the proliferation of CRC via increasing the expression of EXOSC4.