三阴性乳腺癌中与癌性b细胞淋巴瘤11A表达升高相关的转录因子和microrna

N. N. Laqtom, K. Algothmi, Amani H. Bakhribah
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摘要

引证:Laqtom NN, Algothmi KM, Bakhribah AH。三阴性乳腺癌中与癌性b细胞淋巴瘤11A表达升高相关的推断转录因子和microrna中华医学会医学杂志2016;23(3): 9-21。DOI: 10.4197 /地中海。23.3.2摘要b细胞淋巴瘤11A是一种转录抑制因子,在三阴性乳腺癌中高表达。体外研究和动物模型提供了初步证据,表明敲除b细胞淋巴瘤11A对乳腺癌具有治疗作用。明确驱动b细胞淋巴瘤11A高表达的调控因子对于了解其癌症相关功能非常重要。在这些调节因子中,转录因子和microrna对基因表达至关重要,并与表达扰动相关。首先,我们确定了可能与b细胞淋巴瘤11A启动子相互作用的转录因子。基于生物信息学预测和多个组学数据集,发现三阴性乳腺癌中两个上调的转录激活因子Zinc Finger BED-Type Containing 4和E2F Transcription Factor 1在b细胞淋巴瘤11A启动子中有7个位点。其次,我们旨在确定一组可能介导b细胞淋巴瘤11A转录后抑制的microRNA。miR-513a-5p、miR-139-5p、miR1179、miR-140-5p和miR-542-3p至少有一个与b细胞淋巴瘤11a3 '非翻译区相互作用的位点,在三阴性乳腺癌中被发现受到抑制。综上所述,转录因子与microrna的组合调控为进一步研究b细胞淋巴瘤11A在三阴性乳腺癌中的表达水平调控提供了有价值的信息。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Inferring Transcription Factors and microRNAs Associated with Elevated Expression of the Oncogenic B-Cell Lymphoma 11A in Triple Negative Breast Cancer
Citation Laqtom NN, Algothmi KM, Bakhribah AH. Inferring transcription factors and microRNAs associated with elevated expression of the Oncogenic B-Cell Lymphoma 11A in Triple Negative Breast Cancer. JKAU Med Sci 2016; 23 (3): 9-21. DOI: 10.4197/Med. 23.3.2 Abstract B-cell lymphoma 11A, a transcriptional repressor, is highly expressed in triple negative breast cancer. The in vitro studies and animal models provide initial evidence suggesting that the knockdown of B-cell lymphoma 11A has a therapeutic eff ect on breast cancer. Defi ning the regulators driving the high expression of B-cell lymphoma 11A is important to understand its cancer-related functions. Among these regulators, transcription factors and microRNAs are critical for gene expression and associated with expression perturbations. Firstly, we identifi ed the transcription factors that potentially interact with B-cell lymphoma 11A promoter. Based on bioinformatics prediction and multiple Omics datasets, two upregulated transcriptional activators Zinc Finger BED-Type Containing 4 and E2F Transcription Factor 1 in triple negative breast cancer were found to have seven sites within B-cell lymphoma 11A promoter. Secondly, we aimed to determine a putative set of microRNA that can mediate the post-transcriptional repression of B-cell lymphoma 11A. miR-513a-5p, miR-139-5p, miR1179, miR-140-5p, and miR-542-3p, harboring at least one site of interaction with B-cell lymphoma 11A 3' untranslated region, were found inhibited in triple negative breast cancer. Taken together, the combinatorial regulation by transcription factors and microRNAs provide valuable information for further investigation on controlling the expression level of B-cell lymphoma 11A in triple negative breast cancer.
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