Abstract: Objective: To detect the expressions of lncRNA H19(H19) and IL-6/STAT3 pathway in the ulcerative colitis-associated colorectal cancer(CAC) tissue of the mice, and to explore its possible mechanism. Methods: A total of 22 C57BL/6 mice were randomly divided into control group(n=10) and model group(n=12). The CAC models were induced by azomethane(AOM) combined with dextran sodium sulfate(DSS) in the mice in model group. The mice were sacrificed on the 120th day, the disease activity index(DAI) of the mice was evaluated, the tumor formation rate was evaluated,the colon length was measured, and the pathomorphology of colon tissue of the mice was observed by HE staining. The serum IL-6 level of the mice was detected by ELISA.The expression levels of H19, let-7a, IL-6, STAT3 and c-Myc mRNA in colon tissue of the mice were detected by qPCR method.The expression levels of p-STAT3 and c-Myc proteins in colon tissue of the mice were detected by Western blotting method. Results: Compared with control group, the tumor formation rate of the mice in model group was 100%, the colon length was significantly shortened (P<0.01), the DAI score was increased (P<0.01), the colon tissue showed the intraepithelial neoplasia by HE staining,the expression levels of H19, IL-6, STAT3 and c-myc mRNA in colon tissue were significantly increased (P<0.01), the expression level of let-7a mRNA in colon tissue was significantly decreased (P<0.01), the serum IL-6 level was increased (P<0.01), and the expression levels of p-STAT3 and c-Myc proteins in colon tissue were increased (P<0.01). Conclusion: The pathogenesis of CAC in the mice may be related to the up-regulation of c-Myc and H19 and down-regulation of let-7a, which are mediated by IL-6/STAT3 pathway.

Key words: long noncoding RNAs H19, interleukin-6, signal transducer and activator of transcription-3, let-7a, c-Myc, ulcerative colitis, colorectal cancer