Abstract
BackgroundInflammation often induces regeneration to repair the tissue damage. However, chronic inflammation can transform temporary hyperplasia into a fertile ground for tumorigenesis. Here, we demonstrate that the miR-124 acts as a safeguard to inhibit the pro-inflammatory production and reparative regeneration.MethodsThe expression levels of miR-124 and IL-17, IFN-γ were detected by qRT-PCR. TH17 or TH1 cells were detected by flow cytometer, respectively. The binding of STAT3 to the promoter region of IL-17 gene was analyzed by Chip assay. miR-124 binding to the 3′UTR of STAT3 gene was detected by reported plasmid construction and luciferase assay. Furthermore, DSS-induced colitis mice model and T cell transfer model were used to confirm the function of miR-124 in vivo. The related gene expression was analyzed by ELISA and western blot experiments.ResultsThe results indicated that miR-124 decrease promotes colon tumorigenesis after Citrobacter rodentium infection and AOM/DSS induced colon cancer murine model. In molecular mechanism, miR-124 targets STAT3 to inhibit TH17 cell polarization and keep TH17 polarization in colonic microenvironment.ConclusionsOur study strengthened the important role of miR-124 in the regulation of adaptive immune responses and blocking the development of colitis-related cancer.
Highlights
Inflammation often induces regeneration to repair the tissue damage
Purified CD4+ T cells from C57BL/6 mice were subjected to primer in vitro for 3 days under TH0, TH17, Treg and TH1 conditions, and the expression of miR-124 was evaluated by quantitative real-time PCR (qPCR)
We found that miR-124 expression was significantly reduced in TH17 cells but not in TH1 (Figure 1A). qPCR and ELISA experiments showed that miR-124 mimics significantly inhibited the expression of TH17 or TH1 related genes (Figures 1B–E)
Summary
Inflammation often induces regeneration to repair the tissue damage. chronic inflammation can transform temporary hyperplasia into a fertile ground for tumorigenesis. DSS-induced colitis mice model and T cell transfer model were used to confirm the function of miR-124 in vivo. The previous studies confirmed that IL-17 expression step by step increased along with colonic adenomas to cancer process, but it is not a prominent mark to diagnose the CRC because IL-17 is not associated with TNM parameters of the tumor [4, 5]. These results indicated that IL-17 oncogenous function might cooperate with other genes in colon cancer
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