Long non-coding RNA (lncRNA) as a widespread and pivotal epigenetic molecule participates in the occurrence and progression of malignant tumors. DRAIC, a kind of lncRNA whose coding gene location is on 15q23 chromatin, has been found to be weakly expressed in a variety of malignant tumors and acts as a suppressor, but its characteristics and role in gastric cancer (GC) remain to be elucidated. Sixty-seven primary GC tissues and paired paracancerous normal tissues were collected. Bioinformatics is used to predict the interaction molecules of DRAIC. DRAIC and NFRKB were overexpressed or interfered exogenously in GC cells by lentivirus or transient transfection. Quantitative real-time PCR (qPCR) and western blotting were used to evaluate the expression of DRAIC, UCHL5 and NFRKB. The combinations of DRAIC and NFRKB or UCHL5 and NFRKB were verified by RNA-IP and Co-IP assays. Ubiquitination-IP and the treatment of MG132 and CHX were used to detect the ubiquitylation level of NFRKB. The CCK-8 and transwell invasion and migration assays measured the proliferation, migration and invasion of GC cells. DRAIC is down-regulated in GC tissues and cell lines while its potential interacting molecules UCHL5 and NFRKB are up-regulated, and DRAIC is positively correlated with NFRKB protein instead of mRNA. Lower DRAIC and higher UCHL5 and NFRKB indicated advanced progression of GC patients. DRAIC could increase NFRKB protein significantly instead of NFRKB mRNA and UCHL5, and bind to UCHL5. DRAIC combined with UCHL5 and attenuated binding of UCHL5 and NFRKB, meanwhile promoting the degradation of NFRKB via ubiquitination, and then inhibited the proliferation and metastasis of GC cells, which can be rescued by oeNFRKB. DRAIC suppresses GC proliferation and metastasis via interfering with the combination of UCHL5 and NFRKB and mediating ubiquitination degradation.

中文翻译：

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LncRNA DRAIC通过干扰UCHL5介导的NFRKB去泛素化抑制胃癌细胞的增殖和转移。

长链非编码RNA（lncRNA）作为一种广泛存在的关键表观遗传分子参与了恶性肿瘤的发生和发展。DRAIC是一种编码基因定位在15q23染色质上的lncRNA，已被发现在多种恶性肿瘤中弱表达并起抑制作用，但其在胃癌（GC）中的特征和作用仍有待阐明。收集了 67 个原发性 GC 组织和成对的癌旁正常组织。生物信息学用于预测 DRAIC 的相互作用分子。DRAIC 和 NFRKB 通过慢病毒或瞬时转染在 GC 细胞中过表达或受到外源性干扰。定量实时 PCR (qPCR) 和蛋白质印迹用于评估 DRAIC、UCHL5 和 NFRKB 的表达。DRAIC 和 NFRKB 或 UCHL5 和 NFRKB 的组合通过 RNA-IP 和 Co-IP 测定进行验证。泛素化-IP和MG132和CHX处理用于检测NFRKB的泛素化水平。CCK-8 和 transwell 侵袭和迁移测定法测量了 GC 细胞的增殖、迁移和侵袭。DRAIC 在 GC 组织和细胞系中下调，而其潜在的相互作用分子 UCHL5 和 NFRKB 上调，并且 DRAIC 与 NFRKB 蛋白而非 mRNA 呈正相关。较低的 DRAIC 和较高的 UCHL5 和 NFRKB 表明 GC 患者进展较快。DRAIC 可以显着增加 NFRKB 蛋白而不是 NFRKB mRNA 和 UCHL5，并与 UCHL5 结合。DRAIC 与 UCHL5 结合，减弱 UCHL5 与 NFRKB 的结合，同时通过泛素化促进 NFRKB 的降解，然后抑制GC细胞的增殖和转移，可以通过oeNFRKB挽救。DRAIC 通过干扰 UCHL5 和 NFRKB 的组合并介导泛素化降解来抑制 GC 增殖和转移。