Gastric adenocarcinoma (GAC) is one kind of gastric cancer with a high incidence rate and mortality. It is essential to study the etiology of GAC and provide theoretical guidance for the prevention and treatment of GAC. Bioinformatics was used via differential expression analysis, weighted gene co-expression network analysis, gene set enrichment analysis, and a training support vector machine (SVM) model to construct a TSIX/mir-320a/Rad51 network as the research index of GAC disease. On the basis of CRISPR/Cas9 gene editing technology, the present study utilizes the Cation lipid-assisted PEG-6-PLGA polymer nanoparticle (CLAN) drug carrier system to prepare the target knock-out TSIX drug with CRISPR/CaS9 nucleic acid. Knocking down lncRNA TSIX restored the suppression role of miR-320a on Rad51 and inhibited the Rad51 expression. Simultaneously, this ceRNA network activated the ATF6 signaling pathway after endoplasmic reticulum stress to promote GAC cells' apoptosis and inhibit the disease. TSIX/miR-320a/Rad51 network may be a potential biological target of GAC disease and provides a new strategy for treating GAC disease.

中文翻译：

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阳离子脂质辅助 PEG6-PLGA 聚合物纳米颗粒封装的长 ncRNA 通过支持向量机模型逆转 Xist 的非编码 RNA 以调节胃癌细胞凋亡的分子机制。

胃腺癌（GAC）是一种高发病率和高死亡率的胃癌。研究GAC的病因学，为GAC的防治提供理论指导至关重要。通过差异表达分析、加权基因共表达网络分析、基因集富集分析和训练支持向量机（SVM）模型，利用生物信息学构建TSIX/mir-320a/Rad51网络作为GAC疾病的研究指标。本研究在CRISPR/Cas9基因编辑技术的基础上，利用阳离子脂质辅助PEG-6-PLGA聚合物纳米颗粒（CLAN）药物载体系统，制备了具有CRISPR/CaS9核酸的靶向敲除TSIX药物。敲低lncRNA TSIX恢复了miR-320a对Rad51的抑制作用并抑制了Rad51的表达。同时，该ceRNA网络在内质网应激后激活ATF6信号通路，促进GAC细胞凋亡并抑制疾病。TSIX/miR-320a/Rad51网络可能是GAC疾病的潜在生物学靶点，为治疗GAC疾病提供了新的策略。