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Genomic data on breast cancer transcript profile modulation by 17beta-hydroxysteroid dehydrogenase type 1 and 17-beta-estradiol

机译:通过17β-羟基类固醇脱氢酶1和17-β-雌二醇调节乳腺癌基因转录谱的基因组数据

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摘要

The data presented here are related to the research article entitled “Estradiol-independent modulation of breast cancer transcript profile by 17beta-hydroxysteroid dehydrogenase type 1” (J.A. Aka, E.L. Calvo, S.X. Lin, 2016) [1]. We evaluated the effect of the steroidal enzyme 17β-HSD1 and its product, the estrogenic hormone 17-beta-estradiol (E2), on gene transcription profile of breast cancer cells. RNA interference technique was used to knock down the 17β-HSD1 gene (HSD17B1) in the hormone-dependent breast cancer cell line T47D in steroid-deprived medium. Transfected cells were subsequently treated with E2, and microarray analyses (with three contrasts) were used to investigate (i) the effect of 17β-HSD1 expression on breast cancer cell transcript profile in steroid-deprived condition, (ii) the effect of E2 on breast cancer gene expression and (iii) if E2 affects gene regulation by 17β-HSD1. Functional enrichments of the differentially expressed genes were assessed using Ingenuity Pathway Analysis (IPA). Here, we showed data on 140 genes that are induced or repressed 1.5 time or higher (p < 0.05) in the HSD17B1-silenced and E2-treated T47D cells revealed by microarray analysis, and presented the 14 functional terms found in the cancer and in the cell death and survival categories revealed by the IPA biological function analysis. Data on IPA Canonical Pathway and network analyses is also presented. Further discussion on gene regulation by 17β-HSD1 and E2 is provided in the accompanying publication [1].
机译:此处提供的数据与题为“17β-羟基类固醇脱氢酶1型对雌二醇的乳腺癌转录谱谱独立调节”的研究文章有关(J.A. Aka,E.L。Calvo,S.X。Lin,2016)[1]。我们评估了甾体酶17β-HSD1及其产物雌激素17-β-雌二醇(E2)对乳腺癌细胞基因转录谱的影响。 RNA干扰技术用于在激素缺乏的培养基中敲除激素依赖性乳腺癌细胞T47D中的17β-HSD1基因(HSD17B1)。转染的细胞随后用E2处理,并进行了微阵列分析(具有三个对比),用于研究(i)在类固醇缺乏的情况下17β-HSD1表达对乳腺癌细胞转录谱的影响,(ii)E2对乳腺癌基因表达;(iii)E2是否影响17β-HSD1的基因调控。使用Ingenuity Pathway Analysis(IPA)评估差异表达基因的功能富集。在这里,我们显示了通过微阵列分析揭示的在HSD17B1沉默和E2处理的T47D细胞中被诱导或抑制1.5倍或更长时间(p <0.05)的140个基因的数据,并提供了在癌症和IPA生物学功能分析揭示了细胞死亡和存活类别。还介绍了IPA规范途径和网络分析的数据。随附的出版物[1]中提供了关于17β-HSD1和E2调控基因的更多讨论。

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