肺癌占所有癌症相关死亡率的四分之一，是所有癌症中死亡率最高的。尽管癌症治疗方面最近取得了科学进步，但肺腺癌 (LUAD) 癌症患者的 5 年生存率仍然低于 15%。有人认为，LUAD 的高死亡率与获得具有干细胞样特征的祖细胞样细胞有关，这些细胞有助于整个肿瘤调节免疫细胞浸润。为了进一步检验这一假设，本研究挖掘了多个数据库来探索 LUAD 癌症中干性相关基因和 miRNA 的存在。我们检查它们与免疫和辅助细胞浸润率以及患者生存率的关系。我们发现 LUAD 中存在 3 个干细胞相关基因：ORC1L、KIF20A 和 DLGAP5，它们也与免疫浸润率的变化和患者生存率的降低相关。此外，骨髓源性抑制细胞 (MDSC) 浸润的调节以及 miRNA hsa-mir-1247-3p 介导的肿瘤抑制因子 SLC24A4 和癌基因 RAB3B 和 HJURP 的靶向似乎主要调节 LUAD 患者的生存。鉴于这些发现，hsa-mir-1247-3p 和/或其相关基因靶标可能为提高患者的生存能力提供有希望的途径。版权所有：© 2023 Limbu, McCloskey。这是一篇根据知识共享署名许可条款分发的开放获取文章，允许在任何媒体上不受限制地使用、分发和复制，前提是注明原始作者和来源。

Lung cancer makes up one-fourth of all cancer-related mortality with the highest mortality rate among all cancers. Despite recent scientific advancements in cancer therapeutics, the 5-year survival rate of lung adenocarcinoma (LUAD) cancer patients remains below 15 percent. It has been suggested that the high mortality rate of LUAD is linked to the acquisition of progenitor-like cells with stem-like characteristics that assist the whole tumor in regulating immune cell infiltration. To examine this hypothesis further, this study mined several databases to explore the presence of stemness-related genes and miRNAs in LUAD cancers. We examine their association with immune and accessory cell infiltration rates and patient survival. We found 3 stem cell-related genes, ORC1L, KIF20A, and DLGAP5, present in LUAD that also correlate with changes in immune infiltration rates and reduced patient survival rates. Additionally, the modulation in myeloid-derived suppressor cell (MDSC) infiltration and miRNA hsa-mir-1247-3p mediated targeting of tumor suppressor SLC24A4 and oncogenes RAB3B and HJURP appears to primarily regulate LUAD patient survival. Given these findings, hsa-mir-1247-3p and/or its associated gene targets may offer a promising avenue to enhance patient survivability.Copyright: © 2023 Limbu, McCloskey. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.