Objective To study the molecular mechanism that SLC16A8 promotes colorectal cancercell proliferation and angiogenesis through upregulating FN1 expression. Methods Data from The Cancer Genome Atlas were utilized to analyse the expression of SLC16A8 in CRC and the association between SLC16A8 on poor prognosis, and the functional analysis of SLC16A8 was performed by CancerSEA database.RT-qPCR was used to detect the expression of SLC16A8 in CRC cells,and CRC cells were divided into SLC16A8 highly expressed group,blank control group and negative control group, then CCK8 was used to analyze cell proliferation andTranswell assay was used to detect capability of cell migration,Tube formation assay was performed to test the angiogenesis ability.Bioinformatics method was used to screen downstream gene of SLC16A8,and expression of SLC16A8 on FN1 protein were analyzed by western blot.Overexpression of SLC16A8 and inhibition of FN1 and CRC cells were divided into SLC16A8 highly expressed group,SLC16A8 highly expressed group+FN1 siRNA group,blank control group and negative control group,then we analyse whether SLC16A8 promotes cell proliferation, migration and angiogenesis through positive regulating FN1 .Results The results show that the expression of SLC16A8 is overexpressed in CRC,and high expression of SLC16A8 had shorter overall survival (P=0.022)SLC16A8 genes was mainly involved in angiogenesis.SLC16A8 was significantly elevated in the colorectal cancer cell lines, and overexpression of SLC16A8 enhanced cell proliferation, migration and angiogenesis.FN1 might be downstream gene of SLC16A8 and the expression of SLC16A8 was correlated positively with that of FN1 in CRC SLC16A8 promoted FN1 protein expression, and SLC16A8 promotes CRC cell proliferation, migration and angiogenesis through positive regulating FN1.Conclusion SLC16A8 is higher expressed in CRC,and SLC16A8 promotes CRC cell proliferation, migration and angiogenesis through positive regulating FN1