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Unique Haploinsufficient Role of the MicroRNA-Processing Molecule Dicer1 in a Murine Colitis-Associated Tumorigenesis Model

机译：MicroRNA处理分子Dicer1在小鼠结肠炎相关的肿瘤发生模型中的独特Haploinsufficient作用。

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A widespread downregulated expression of microRNAs (miRNAs) is commonly observed in human cancers. Similarly, deregulated expression of miRNA-processing pathway components, which results in the reduction of global miRNA expression, may also be associated with tumorigenesis. Here, we show that specific ablation of Dicer1 in intestinal epithelial cells accelerates intestinal inflammation-associated tumorigenesis. This effect was apparent only when a single copy of Dicer1 was deleted, but not with complete Dicer1 ablation. DICER expression and subsequent mature miRNA levels were inversely correlated with the number of intact Dicer1 alleles. Because the expression levels of DICER were retained in tumors and its surrounding tissues even after induction of colitis-associated tumors, the effects of Dicer1 deletion were cell-autonomous. Although the expression levels of representative oncogenes and tumor suppressor genes were in most cases inversely correlated with the expression levels of DICER, some genes were not affected by Dicer1 deletion. Thus, deregulating the delicate balance between the expression levels of tumor-promoting and -suppressive genes may be crucial for tumorigenesis in this unique haploinsufficient case.
机译：在人类癌症中通常观察到广泛下调的microRNA（miRNA）表达。类似地，导致整体miRNA表达减少的miRNA加工途径成分的表达失调也可能与肿瘤发生有关。在这里，我们显示Dicer1在肠上皮细胞中的特异性消融加速了肠道炎症相关的肿瘤发生。仅当删除Dicer1的单个副本时，此效果才明显，但没有完全Dicer1消融时，此效果不明显。 DICER表达和随后的成熟miRNA水平与完整Dicer1等位基因的数量成反比。因为即使在诱发结肠炎相关肿瘤后，DICER的表达水平仍保留在肿瘤及其周围组织中，所以Dicer1缺失的作用是细胞自主的。尽管在大多数情况下，代表性癌基因和抑癌基因的表达水平与DICER的表达水平呈负相关，但某些基因不受Dicer1缺失的影响。因此，在这种独特的单倍不足的情况下，解除促肿瘤基因和抑癌基因表达水平之间微妙的平衡可能对于肿瘤发生至关重要。

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