The MicroRNAmiR-223constrains Colitis-associated tumorigenesis by limiting myeloid cell infiltration and Chemokine expression. The MicroRNAmiR-223constrains Colitis-associated tumorigenesis by limiting myeloid cell infiltration and Chemokine expression

Aberrant intestinal inflammation plays a critical role in the development of colitis-associated colorectal cancer (CAC), yet the mechanisms behind this progression are not clearly defined. While altered microRNA (miRNA) expression is observed in CAC, it is unclear how myeloid-specific microRNA’s impact on the inflammatory process that underpins the continuum from Ulcerative colitis (UC) to tumorigenesis. Here we used the Azoxymethane-Dextran Sodium Sulfate (AOM-DSS) (10mg/kg) model of CAC on miR-223-/y and WT mice, with an overall aim of identifying differences in their expression profiles following AOM/DSS treatment. Overall design: To investigate the effects of miR-223 on the development of colitis associated colorectal cancer, we used miR-223-/y and C57BL/6J mice treated with azoxymethane(AOM)/dextran sodium sulfate(DSS) (10mg/kg). Total RNA was extracted from colonic tissue and gene expression analysis was performed on RNA-seq results.

异常肠道炎症在结肠炎相关结直肠癌（colitis-associated colorectal cancer，CAC）的发生发展中扮演关键角色，然而该病程进展的具体分子机制尚未阐明。尽管结肠炎相关结直肠癌中已观测到微小核糖核酸（microRNA，miRNA）表达异常，但髓系特异性微小核糖核酸如何调控从溃疡性结肠炎（Ulcerative colitis，UC）向肿瘤发生发展的连续性炎症过程，目前仍不明确。
本研究采用氧化偶氮甲烷-葡聚糖硫酸钠（Azoxymethane-Dextran Sodium Sulfate，AOM-DSS，10mg/kg）构建结肠炎相关结直肠癌模型，对miR-223-/y小鼠与野生型（WT）小鼠进行处理，整体研究目标为明确AOM/DSS造模后二者的基因表达谱差异。
总体实验设计：为探究miR-223对结肠炎相关结直肠癌发生发展的影响，本研究对miR-223-/y小鼠与C57BL/6J野生型小鼠施以氧化偶氮甲烷（azoxymethane，AOM）/葡聚糖硫酸钠（dextran sodium sulfate，DSS，10mg/kg）处理。从结肠组织中提取总RNA，并基于RNA测序结果开展基因表达分析。