ABSTRACT
Objective To explore the effect of LINC00115 targeting miR-874-3p on the biological behavior and paclitaxel sensitivity of liver cancer cells.Methods The qRT-PCR was performed to detect the expression levels of LINC00115 and miR-874-3p in liver cancer tissues and cell lines.The si-NC,si-LINC00115,miR-NC,miR-874-3p,pcDNA,pcDNA-LINC00115,anti-miR-NC+si-LINC00115,anti-miR-874-3p+si-LINC00115 were transfected into liver cancer cells MHCC97H respective-ly.CCK-8 method was applied to assess cell viability and IC50 value to paclitaxel.Transwell assay was performed to detect cell migration and invasion.Dual luciferase reporter gene method was used to determine the relationship between LINC00115 and miR-874-3p.Results LINC00115 was highly expressed(P＜0.05),while miR-874-3p was lowly expressed(P＜0.05)in liver cancer tissues and cell lines.After downregulating LINC00115,the cell absorbance(A)value,the IC50 value to paclitaxel,migra-tion and invasion were significantly reduced(all P＜0.05),while miR-874-3p expression was significantly increased(P＜0.05).After upregulating miR-874-3p,the cell A value,IC50 value to paclitaxel,migration and invasion were significantly reduced(all P＜0.05).After upregulating LINC00115,miR-874-3p expression was decreased(P＜0.05).LINC00115 had a direct interaction with miR-874-3p.Downregulating miR-874-3p significantly reduced the effect of low LINC00115 expression on A value,IC50 value to paclitaxel,migration and invasion of liver cancer cells(all P＜0.05).Conclusion Downregulation of LINC00115 inhibits the prolifera-tion,migration and invasion of liver cancer cells to increase paclitaxel sensitivity by promoting miR-874-3p expression.
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.