〔Abstract〕 Objective To explore the mechanism of exosome-derived LncRNA ESCCAL-1 regulating the miR-874/ITGBL1 axis in the progression of colorectal cancer(CRC). Methods The differentially expressed genes in CRC were analyzed using the Gene Expression Omnibus(GEO) database. Expressions of LncRNA ESCCAL-1,miR-874 and ITGBL1 in CRC tissues and cell lines(SW480,SW620,HCT116 and HT29) and adjacent normal tissues and NCM460 cell lines were detected by qRT-PCR; 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyltetrazoliumbromide(MTT),clone formation and flow cytometry was used to detect cell proliferation,colony formation and apoptosis;dual luciferase reporter assays were used to verify the interaction between miR-874 and ESCCAL-1,ITGBL1; fluorescence in situ hybridization was used to determine the subcellular localization of LncRNAESCCAL-1. Exosomes were isolated from serum using the Exosome extraction kit. Results The expressions of ESCCAL-1 and ITGBL1 in CRC tissues and cell lines were higher than those in adjacent normal tissues and NCM460 cell lines,while the opposite was true for miR-874(P<0. 05). Knockdown of ESCCAL-1 can inhibit CRC cell proliferation and colony formation and promote apoptosis. There are specific binding sites for miR-874 and ESCCAL-1,and miR-874 inhibitor could partially reverse the effect of knockdown ESCCAL-1 in CRC(P<0. 05). ESCCAL-1 upregulates ITGBL1 by adsorbing miR-874. The serum levels of ESCCAL-1 and exo-ESCCAL-1 in CRC patients were higher than those in the control group. Serum exo-ESCCAL-1 may be a valuable diagnostic indicator for CRC treatment(P<0. 05).Conclusion ESCCAL-1 promotes CRC progression by regulating the miR-874/ITGBL1 axis,and ESCCAL-1 may be an effective molecular target for CRC therapy.