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 ) -2，5diphenyltetrazoliumbromide (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 formiR-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.