Long non‐coding RNAs (lncRNAs) are key regulators or a range of diseases and chronic conditions such as cancers, but how they function in the context of ovarian cancer (OC) is poorly understood. The Coding‐Potential Assessment Tool was used to assess the likely protein‐coding potential of SNHG7. SNHG7 expression was elevated in ovarian tumour tissues measured by qRT‐PCR. The online database JASPAR was used to predict the transcription factors binding to SNHG7. Twenty‐four‐well Transwell plates were used for invasion assays. RNA immunoprecipitation was performed to determine RNA‐protein associations. EdU assay was introduced to detect cell proliferation. Chromatin immunoprecipitation was performed to confirm the directly interaction between DNA and protein. We discovered that in the context of OC there is a significant up‐regulation of the lncRNA SNHG7. Knocking down this lncRNA disrupted both OC cell invasion and proliferation, while its overexpression had the opposite effect. SP1 binding sites were present in the SNHG7 promoter, and chromatin immunoprecipitation (ChIP) confirmed direct SP1 binding to this region, activating SNHG7 transcription. We found that at a mechanistic level in OC cells, KLF2 is a probable SNHG7 target, as we found that SHNCCC16 directly interacts with EZH2 and thus represses KLF2 expression. In summary, this research demonstrates that lncRNA SNHG7 is an SP1‐activated molecule that contributes to OC progression by providing a scaffold whereby EZH2 can repress KLF2 expression.

中文翻译：

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较长的非编码RNA SNGH7被SP1激活，并通过与EZH2相互作用在卵巢癌中发挥致癌作用。

较长的非编码RNA（lncRNA）是关键调控因子或一系列疾病和慢性病，例如癌症，但人们对它们在卵巢癌（OC）中的功能了解甚少。编码潜能评估工具用于评估SNHG7可能的蛋白质编码潜能。通过qRT-PCR测定，SNHG7在卵巢肿瘤组织中表达升高。在线数据库JASPAR用于预测与SNHG7结合的转录因子。使用二十四孔Transwell板进行侵袭测定。进行RNA免疫沉淀以确定RNA与蛋白质的结合。引入EdU分析来检测细胞增殖。进行了染色质免疫沉淀，以确认DNA和蛋白质之间的直接相互作用。我们发现在OC的背景下，lncRNA SNHG7明显上调。敲低该lncRNA破坏了OC细胞的侵袭和增殖，而其过表达却产生了相反的作用。SP1结合位点存在于SNHG7启动子中，染色质免疫沉淀（ChIP）证实SP1直接与该区域结合，从而激活SNHG7转录。我们发现在OC细胞中的机制水平上，KLF2是可能的SNHG7靶标，因为我们发现SHNCCC16直接与EZH2相互作用，从而抑制KLF2的表达。总而言之，这项研究表明lncRNA SNHG7是一种SP1激活的分子，通过提供EZH2可以抑制KLF2表达的支架来促进OC进展。而其过表达则相反。SP1结合位点存在于SNHG7启动子中，染色质免疫沉淀（ChIP）证实SP1直接与该区域结合，从而激活SNHG7转录。我们发现，在OC细胞的机制水平上，KLF2可能是SNHG7的靶标，因为我们发现SHNCCC16与EZH2直接相互作用，从而抑制KLF2的表达。总而言之，这项研究表明lncRNA SNHG7是一种SP1激活的分子，通过提供EZH2可以抑制KLF2表达的支架来促进OC进展。而其过表达则相反。SP1结合位点存在于SNHG7启动子中，染色质免疫沉淀（ChIP）证实SP1直接与该区域结合，从而激活SNHG7转录。我们发现在OC细胞中的机制水平上，KLF2是可能的SNHG7靶标，因为我们发现SHNCCC16直接与EZH2相互作用，从而抑制KLF2的表达。总而言之，这项研究表明lncRNA SNHG7是一种SP1激活的分子，通过提供EZH2可以抑制KLF2表达的支架来促进OC进展。KLF2是可能的SNHG7靶标，因为我们发现SHNCCC16与EZH2直接相互作用，因此抑制KLF2表达。总而言之，这项研究表明lncRNA SNHG7是一种SP1激活的分子，通过提供EZH2可以抑制KLF2表达的支架来促进OC进展。KLF2是可能的SNHG7靶标，因为我们发现SHNCCC16与EZH2直接相互作用，因此抑制KLF2表达。总而言之，这项研究表明lncRNA SNHG7是一种SP1激活的分子，通过提供EZH2可以抑制KLF2表达的支架来促进OC进展。