Differential Expression of Super-Enhancer-Associated Long Non-coding RNAs in Uterine Leiomyomas.
Differential Expression of Super-Enhancer-Associated Long Non-coding RNAs in Uterine Leiomyomas.
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DOI：
10.1007/s43032-022-00981-4
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发表时间：
2022-10
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超增强子相关长链非编码RNA（Super-enhancer-associated long non-coding RNAs，SE-lncRNA）是一类由超增强子（super-enhancer，SE）基因组区域转录的特异性lncRNA。近年来的研究表明，SE-lncRNA通过调控癌基因在肿瘤发生中发挥重要作用。本研究的目的是阐明SE-lncRNA的表达谱，同时评估平滑肌瘤和配对子宫肌层中相关的mRNA。采用Arraystar SE-lncRNA芯片系统分析8例子宫平滑肌瘤和配对子宫肌层中差异表达的SE-lncRNA沿着相应的SE调节蛋白编码基因。分析表明7680个SE-lncRNA表达，其中721个SE-lncRNA过表达，而247个SE-lncRNA在平滑肌瘤中表达不足1.5倍或更多。选择13个新的SE-lncRNA及其相应的蛋白编码基因，并通过定量实时PCR证实它们在81对平滑肌瘤组织中的表达。13对SE-lncRNA及其相应的蛋白编码基因包括RP 11 -353N14.2/CBX 4、SOCS 2-AS 1/SOCS 2、RP 1 -170O19.14/HOXA 11、CASC 15/PRL、EGFLAM-AS 1/EGFLAM、RP 11 - 225 H22/NEURL 1、RP 5 -1086K13.1/CD 58、AC092839.3/SPTBN 1、RP 11 -69I8.3/CTGF、TM 4SF 1-AS 1/TM 4SF 1、RP11-373D23/FOSL 2、RP11-399K21.11/COMTD 1和CTB-113P19.1/FOSL。在这些SE-lncRNA中，与高加索人相比，非裔美国人中SOCS 2-AS 1/SOCS 2、RP 11 -353N14.2/CBX 4、RP 1 -170O19.14/HOXA 11和RP 11 - 225 H22/NEURL 1的表达显著更高。与MED 12突变阴性肿瘤相比，MED 12突变阳性肿瘤中RP 11 - 353 N14.2/CBX 4、SOCS 2-AS 1/SOCS 2、CASC 15/PRL和CTB-113 P19.1/PRL的表达显著更高。总的来说，我们的研究结果表明，平滑肌瘤中SE的差异表达是导致平滑肌瘤中蛋白编码基因失调的另一种机制，并且种族和MED 12突变可以影响一组选择的SE的表达。在线版本包含补充材料，可通过10.1007/s43032-022-00981-4获得。
Super-enhancer-associated long non-coding RNAs (SE-lncRNAs) are a specific set of lncRNAs transcribed from super-enhancer (SE) genomic regions. Recent studies have revealed that SE-lncRNAs play essential roles in tumorigenesis through the regulation of oncogenes. The objective of this study was to elucidate the expression profile of SE-lncRNAs with concurrent assessment of associated mRNAs in leiomyomas and paired myometrium. Arraystar SE-lncRNAs arrays were used to systematically profile the differentially expressed SE-lncRNAs along with the corresponding SE-regulated protein coding genes in eight leiomyomas and paired myometrium. The analysis indicated 7680 SE-lncRNAs were expressed, of which 721 SE-lncRNAs were overexpressed, while 247 SE-lncRNAs were underexpressed by 1.5-fold or greater in leiomyoma. Thirteen novel SE-lncRNAs and their corresponding protein coding genes were selected, and their expression was confirmed in eighty-one paired leiomyoma tissues by quantitative real-time PCR. The thirteen pairs of SE-lncRNAs and their corresponding protein coding genes included RP11-353N14.2/CBX4, SOCS2-AS1/SOCS2, RP1-170O19.14/HOXA11, CASC15/PRL, EGFLAM-AS1/EGFLAM, RP11-225H22/NEURL1, RP5-1086K13.1/CD58, AC092839.3/SPTBN1, RP11-69I8.3/CTGF, TM4SF1-AS1/TM4SF1, RP11-373D23/FOSL2, RP11-399K21.11/COMTD1, and CTB-113P19.1/SPARC. Among these SE-lncRNAs, the expression of SOCS2-AS1/SOCS2, RP11-353N14.2/CBX4, RP1-170O19.14/HOXA11, and RP11-225H22/NEURL1 was significantly higher in African Americans as compared with Caucasians. The expression of RP11-353N14.2/CBX4, SOCS2-AS1/SOCS2, CASC15/PRL, and CTB-113P19.1/SPARC was significantly higher in tumors with MED12-mutation-positive as compared with MED12-mutation-negative tumors. Collectively, our results indicate that the differential expression of SE in leiomyomas is another mechanism contributing to dysregulation of protein coding genes in leiomyomas and that race and MED12 mutation can influence the expression of a select group of SE. The online version contains supplementary material available at 10.1007/s43032-022-00981-4.
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