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通过 Ingenuity 通路分析对三阴性乳腺癌细胞上皮-间质转化中涉及的差异基因表达和核心经典通路进行分析。

Analysis of Differential Gene Expression and Core Canonical Pathways Involved in the Epithelial to Mesenchymal Transition of Triple Negative Breast Cancer Cells by Ingenuity Pathway Analysis.

作者信息

Cagle Elizabeth, Lake Brent, Banerjee Anasua, Cuffee Jazmine, Banerjee Narendra, Gilmartin Darla, Liverman Makaiyah, Brown Shennel, Armstrong Erik, Bhattacharya Santanu, Ghosh Somiranjan, Mandal Tanmoy, Banerjee Hirendra

机构信息

Department of Natural, Health and Human Sciences, Elizabeth City State University Campus of The University of North Carolina, Elizabeth, NC, USA.

Department of Biochemistry and Molecular Biology, Mayo College of Medicine and Science, Jacksonville, FL, USA.

出版信息

Comput Mol Biosci. 2023 Jun;13(2):21-34. doi: 10.4236/cmb.2023.132002. Epub 2023 May 19.

Abstract

Triple Negative Breast Cancer (TNBC) is a malignant form of cancer with very high mortality and morbidity. Epithelial to Mesenchymal Transition (EMT) is the most common pathophysiological change observed in cancer cells of epithelial origin that promotes metastasis, drug resistance and cancer stem cell formation. Since the information regarding differential gene expression in TNBC cells and cell signaling events leading to EMT is limited, this investigation was done by comparing transcriptomic data generated by RNA isolation and sequencing of a EMT model TNBC cell line in comparison to regular TNBC cells. RNA sequencing and Ingenuity Pathway Software Analysis (IPA) of the transcriptomic data revealed several upregulated and downregulated gene expressions along with novel core canonical pathways including Sirtuin signaling, Oxidative Phosphorylation and Mitochondrial dysfunction events involved in EMT changes of the TNBC cells.

摘要

三阴性乳腺癌(TNBC)是一种恶性癌症,死亡率和发病率都非常高。上皮-间质转化(EMT)是在上皮来源的癌细胞中观察到的最常见的病理生理变化,它会促进转移、耐药性和癌症干细胞的形成。由于关于TNBC细胞中差异基因表达以及导致EMT的细胞信号事件的信息有限,本研究通过比较EMT模型TNBC细胞系与常规TNBC细胞经RNA分离和测序产生的转录组数据来进行。转录组数据的RNA测序和 Ingenuity Pathway软件分析(IPA)揭示了几种上调和下调的基因表达,以及包括Sirtuin信号传导、氧化磷酸化和线粒体功能障碍事件在内的新的核心经典途径,这些途径参与了TNBC细胞的EMT变化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f01/10398793/16af76363547/nihms-1910794-f0001.jpg

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