Yong-Xia Wang1, Yong-Zhen Li1, Wen-Li Zhao1, Zhe-Ying Zhang1, Xin-Lai Qian2, Guo-Yang He3. 1. Department of Pathology, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang 453003, Henan, China; Department of Pathology, The Third Affiliated Hospital of Xinxiang Medical University, Xinxiang 453003, Henan, China; Henan Provincial Key Laboratory of Molecular Oncologic Pathology, Henan, Xinxiang, China. 2. Department of Pathology, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang 453003, Henan, China; Department of Pathology, The Third Affiliated Hospital of Xinxiang Medical University, Xinxiang 453003, Henan, China; Henan Provincial Key Laboratory of Molecular Oncologic Pathology, Henan, Xinxiang, China. Electronic address: qxlsfyblk@126.com. 3. Department of Pathology, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang 453003, Henan, China; Department of Pathology, The Third Affiliated Hospital of Xinxiang Medical University, Xinxiang 453003, Henan, China; Henan Provincial Key Laboratory of Molecular Oncologic Pathology, Henan, Xinxiang, China. Electronic address: hegy3029123@126.com.
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 the 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.
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 the 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.