miR-124-2、miR-92-A1和miR-372在导管原位癌(DCIS)向微浸润性乳腺癌(MIBC)进展的数学模型中调控差异基因表达

Chinchilla-Monge Ricardo, Chaves-Chaves Noe, Mora-Rodriguez Rodrigo
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引用次数: 0

摘要

乳腺癌是一种被广泛研究的遗传性疾病,在初始阶段(从非典型导管增生发展到导管原位癌)和(尽管不一定)浸润性乳腺癌之间有明确的区分。尽管如此,如果浸润性乳腺癌仅在健康乳腺中定植少于1mm,则可归类为微浸润性乳腺癌。我们假设早期癌肿瘤细胞中的差异表达基因受到特定mirna和TF的调控,从而刺激肿瘤进展到侵袭阶段。我们的主要目标是建立一个最小的模型来解释这种行为,并确定具有治疗潜力的有希望的miRNA靶点。使用BioNetUCR和COPASI系统生物学方法,我们确定了miRNAs miR-372, miR-124-2和miR-92-A1在MIBC阶段修改差异基因表达。这些mirna有潜力作为未来治疗策略的治疗靶点,通过抑制从DCIS到IBC的转变。关于DCIS到MIBC转换的研究很少,但是通过这种计算方法,我们提出了这种类型细胞转换的第一个计算机模型之一。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
miR-124-2, miR-92-A1 and miR-372 regulate differential gene expression in a mathematical model of the progression of ductal carcinoma in situ (DCIS) to microinvasive breast cancer (MIBC)
Breast cancer is a widely studied genetic disease that has a clear division between an initial stage, starting with the atypical ductal hyperplasia progressing to ductal carcinoma in situ and ending, although not necessarily, with invasive breast cancer. Nonetheless, if the invasive breast cancer has only colonized less than 1mm of healthy estroma it is classified as microinvasive breast carcinoma. We hypothesized that differentially expressed genes in tumoral cells of early carcinoma are regulated by specific miRNAs and TF that stimulate the progression to an invasive stage. Our main goal was to reach a minimal model that can explain this behavior and identify promising miRNA targets with therapeutic potential. Using BioNetUCR and COPASI for a systems biology approach, we identified miRNAs miR-372, miR-124-2 and miR-92-A1 that modify the differential gene expression in MIBC stage. These miRNAs have potential as therapeutic targets for future treatment strategies by suppressing the transition from DCIS to IBC. There are few studies about DCIS to MIBC transition, but with this computational approach we present one of the first in silico models for this type of cell transition.
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