BACKGROUND In patients with colorectal cancer(CRC),tumour metastasis is the leading cause of death.The search for key genes involved in metastasis of CRC is imperative for improved prognoses and treatments.SPDL1 has b...BACKGROUND In patients with colorectal cancer(CRC),tumour metastasis is the leading cause of death.The search for key genes involved in metastasis of CRC is imperative for improved prognoses and treatments.SPDL1 has been implicated in the deve-lopment of CRC,however,its mechanism of action remains unclear.AIM To investigate the role and mechanism of action by which SPDL1 inhibits the development and metastasis of CRC.METHODS In this study,we examined the relationship between SPDL1 expression and CRC prognosis using immunohistochemistry.Survival analyses were performed using Kaplan-Meier analysis and log-rank test.After knocking down SPDL1 in the HCT116 cancer cell line changes in cell viability,migration,invasion,and gene expression were examined using a cell counting kit 8 assay,Transwell assay,and Western blot.The effect of SPDL1 on the cell cycle was assessed using flow cy-tometry.RNA sequencing was used to analyse the effect of SPDL1 on gene expression of CRC cells.The mechanism of action of SPDL1 in CRC was further clarified using U0126,an inhibitor of the mitogen-activated protein kinase signaling pathway.RESULTS SPDL1 is expressed at low levels in tissues of patients with CRC,and this reduced expression is associated with poor prognosis.Functionally,low expression of SPDL1 in CRC promotes cell proliferation,migration,invasion,and affects the cell cycle.Mechanistically,SPDL1 affects the progression of CRC through its regulation of the process of epithelial-mesenchymal transition(EMT)and of the epidermal growth factor receptor(EGFR)/extracellular signal-regulated kinase(ERK)signaling pathways.CONCLUSION This study showed that the loss of SPDL1 may induce EMT and promote cell migration and invasion in CRC through the EGFR/ERK pathway.展开更多
基金Supported by the Natural Science Foundation of Guangxi Province,No.2019GXNSFAA185030 and No.2023GXNSFBA026129the Scientific Research Project of the Second Affiliated Hospital of Guangxi Medical University,No.EFYKY2020013the Cultivation Science Foundation of the Second Affiliated Hospital of Guangxi Medical University,No.GJPY2023005 and No.GJPY2023009.
文摘BACKGROUND In patients with colorectal cancer(CRC),tumour metastasis is the leading cause of death.The search for key genes involved in metastasis of CRC is imperative for improved prognoses and treatments.SPDL1 has been implicated in the deve-lopment of CRC,however,its mechanism of action remains unclear.AIM To investigate the role and mechanism of action by which SPDL1 inhibits the development and metastasis of CRC.METHODS In this study,we examined the relationship between SPDL1 expression and CRC prognosis using immunohistochemistry.Survival analyses were performed using Kaplan-Meier analysis and log-rank test.After knocking down SPDL1 in the HCT116 cancer cell line changes in cell viability,migration,invasion,and gene expression were examined using a cell counting kit 8 assay,Transwell assay,and Western blot.The effect of SPDL1 on the cell cycle was assessed using flow cy-tometry.RNA sequencing was used to analyse the effect of SPDL1 on gene expression of CRC cells.The mechanism of action of SPDL1 in CRC was further clarified using U0126,an inhibitor of the mitogen-activated protein kinase signaling pathway.RESULTS SPDL1 is expressed at low levels in tissues of patients with CRC,and this reduced expression is associated with poor prognosis.Functionally,low expression of SPDL1 in CRC promotes cell proliferation,migration,invasion,and affects the cell cycle.Mechanistically,SPDL1 affects the progression of CRC through its regulation of the process of epithelial-mesenchymal transition(EMT)and of the epidermal growth factor receptor(EGFR)/extracellular signal-regulated kinase(ERK)signaling pathways.CONCLUSION This study showed that the loss of SPDL1 may induce EMT and promote cell migration and invasion in CRC through the EGFR/ERK pathway.
