肺腺癌（LUAD）是一种非小细胞癌。核糖核酸酶/血管生成素抑制剂 1 (RNH1) 在病毒性癌症中发挥多种作用。 E2F1 是参与 LUAD 发育的关键转录因子。在这里，我们分析了 LUAD 患者中 RNH1 的表达，研究了 RNH1 在 LUAD 中的生物学功能，并通过 LUAD 中的 E2F1 展示了其潜在机制。在本研究中，我们基于数据库呈现了 LUAD 中 RNH1 的表达，并证实了通过蛋白质印迹法检测人 LUAD 组织中的 RNH1。构建慢病毒感染以沉默或过度表达 NCI-H1395 和 NCI-H1437 细胞中的 RNH1。我们通过 MTT 测定、集落形成测定和细胞周期检测评估 RNH1 对 LUAD 细胞增殖的作用。采用Hoechst染色和流式细胞术评价RNH1对LUAD细胞凋亡的影响。通过Transwell实验研究RNH1在侵袭和迁移中的功能。通过双荧光素酶测定、ChIP 检测和 Pull-down 测定来探讨 E2F1 在维持 RNH1 表达和功能中的关联。探讨E2F1对LUAD细胞中RNH1功能的调节。进行小鼠实验以证实 RNH1 在 LUAD 中的体内作用。 mRNA测序表明RNH1过表达改变了LUAD细胞的表达谱。本工作介绍了患者LUAD组织中的RNH1表达。重要的是，RNH1敲低提高了细胞的增殖、迁移和侵袭能力，而RNH1过表达则产生相反的效果。双荧光素酶实验证明E2F1与RNH1启动子(-1064∼-1054,-1514∼-1504)结合，降低RNH1的转录活性。 ChIP 分析表明 E2F1 DNA 在 RNH1 启动子 (-1148 ∼ -943, -1628 ∼ -1423) 处富集。 Pull-down 分析还显示了 E2F1 和 RNH1 启动子 (-1148 ∼ -943) 之间的关联。 E2F1过表达导致了LUAD细胞的恶性行为，而RNH1过表达则逆转了这种行为。高通量测序表明，RNH1 过表达诱导多个基因表达变化，从而调节 LUAD 相关过程。我们的研究表明，E2F1 与 RNH1 启动子结合可能导致 RNH1 表达抑制，从而促进 LUAD 的发展。© 2024。作者。

Lung adenocarcinoma (LUAD) is a non-small cell carcinoma. Ribonuclease/angiogenin inhibitor 1 (RNH1) exerts multiple roles in virous cancers. E2F1 is a critical transcription factor involved in the LUAD development. Here, we analyze the expression of RNH1 in LUAD patients, investigate the biological function of RNH1 in LUAD, and demonstrate its potential mechanisms through E2F1 in LUAD.In the present study, we presented the expression of RNH1 in LUAD based on the database and confirmed it by western blot detection of RNH1 in human LUAD tissues. Lentiviral infection was constructed to silence or overexpress RNH1 in NCI-H1395 and NCI-H1437 cells. We assess the role of RNH1 on proliferation in LUAD cells by MTT assay, colony formation assays, and cell cycle detection. Hoechst staining and flow cytometry were used to evaluate the effects of RNH1 on apoptosis of LUAD cells. The function of RNH1 in invasion and migration was investigated by Transwell assay. Dual luciferase assay, ChIP detection, and pull-down assay were conducted to explore the association of E2F1 in the maintenance of RNH1 expression and function. The regulation of E2F1 on the functions of RNH1 in LUAD cells was explored. Mouse experiments were performed to confirm the in-vivo role of RNH1 in LUAD. mRNA sequencing indicated that RNH1 overexpression altered the expression profile of LUAD cells.RNH1 expression in LUAD tissues of patients was presented in this work. Importantly, RNH1 knockdown improved the proliferation, migration and invasion abilities of cells and RNH1 overexpression produced the opposite effects. Dual luciferase assay proved that E2F1 bound to the RNH1 promoter (-1064 ∼ -1054, -1514 ∼ -1504) to reduce the transcriptional activity of RNH1. ChIP assay indicated that E2F1 DNA was enriched at the RNH1 promoter (-1148 ∼ -943, -1628 ∼ -1423). Pull-down assays also showed the association between E2F1 and RNH1 promoter (-1148 ∼ -943). E2F1 overexpression contributed to the malignant behavior of LUAD cells, while RNH1 overexpression reversed it. High-throughput sequencing showed that RNH1 overexpression induced multiple genes expression changes, thereby modulating LUAD-related processes.Our study demonstrates that binding of E2F1 to the RNH1 promoter may lead to inhibition of RNH1 expression and thus promoting the development of LUAD.© 2024. The Author(s).