Nuclear factors of activated T-cells (NFATs) have been mainly characterized in the context of immune response regulation because, as transcription factors, they have the ability to induce gene transcription. NFAT proteins are found in several types of tumors, for instance, pancreatic carcinoma. The role of NFATs in carcinogenesis is regulating central genes in cell differentiation and cell growth. NFAT proteins are primarily located in cytoplasm and only transported to the cell nucleus after activation. Here, they interact with other transcription factors cooperating with NFAT proteins, thus influencing the selection and regulation of NFAT-controlled genes. To identify and characterize possible interaction partners of the transcription factor NFATc2 in pancreatic carcinoma cells PaTu 8988t. NFATc2 expression and the mode of action of Ionomycin in the pancreatic tumor cell lines PaTu 8988t were shown with Western blotting and immunofluorescence tests. Potential partner proteins were verified by means of immunoprecipitation and binding partners, their physical interactions with DNA pull-down assays, siRNA technologies, and GST pull-down assays. Functional evidence was complemented by reporter–promoter analyses. NFATc2 and Sp1 are co-localized in cell nuclei and physically interact at the NFAT target sequence termed NFAT-responsive promotor construct. Sp1 increases the functional activity of its binding partner NFATc2. This interaction is facilitated by Ionomycin in the early stimulation phase (up to 60 min). Oncological therapy concepts are becoming more and more specific, aiming at the efficient modulation of specific signal and transcription pathways. The oncogenic transcription partner Sp1 is important for the transcriptional and functional activity of NFATc2 in pancreatic carcinoma. The binding partners interact in cells. Further studies are necessary to identify the underlying mechanisms and establish future therapeutic options for treating this aggressive type of tumor.

中文翻译：

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NFATc2和转录因子Sp1在胰腺癌细胞PaTu 8988t中的相互作用。

活化T细胞（NFAT）的核因子主要是在免疫应答调节的背景下表征的，因为它们作为转录因子具有诱导基因转录的能力。NFAT蛋白存在于多种类型的肿瘤中，例如胰腺癌。NFAT在致癌作用中的作用是调节细胞分化和细胞生长中的中心基因。NFAT蛋白主要位于细胞质中，仅在激活后才转运到细胞核。在这里，它们与与NFAT蛋白协同作用的其他转录因子相互作用，从而影响NFAT调控基因的选择和调控。为了鉴定和表征胰腺癌细胞PaTu 8988t中转录因子NFATc2可能的相互作用伴侣。通过蛋白质印迹和免疫荧光测试显示了胰腺癌细胞系PaTu 8988t中NFATc2的表达和伊诺霉素的作用方式。潜在的伴侣蛋白通过免疫沉淀和结合伴侣，它们与DNA下拉测定法，siRNA技术和GST下拉测定法的物理相互作用进行了验证。功能性证据得到了记者-启动子分析的补充。NFATc2和Sp1共定位在细胞核中，并在称为NFAT响应启动子构建体的NFAT目标序列上发生物理相互作用。Sp1增加了其结合伴侣NFATc2的功能活性。碘霉素在早期刺激阶段（长达60分钟）促进了这种相互作用。肿瘤治疗概念变得越来越具体，旨在有效调节特定信号和转录途径。致癌转录伴侣Sp1对于NFATc2在胰腺癌中的转录和功能活性很重要。结合伴侣在细胞中相互作用。有必要进行进一步的研究以确定潜在的机制并建立治疗这种侵略性肿瘤的未来治疗选择。