SLC2A基因家族作为肺腺癌患者诊断标志物和治疗靶点的生物信息学分析数据表

数据集获取（Figshare）

• 源站标题：DataSheet1_SLC2As as diagnostic markers and therapeutic targets in LUAD patients through bioinformatic analysis.docx
• DOI：10.3389/fphar.2022.1045179.s001
• 发布日期：2022-11-28
• 文件数：1 个
• 文件总体积：3.22 MB
• 源站页面：https://frontiersin.figshare.com/articles/dataset/DataSheet1_SLC2As_as_diagnostic_markers_and_therapeutic_targets_in_LUAD_patients_through_bioinformatic_analysis_docx/21627524

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curl -L -o "DataSheet1_SLC2As as diagnostic markers and therapeutic targets in LUAD patients through bioinformatic analysis.docx" "https://ndownloader.figshare.com/files/38341478"

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• DataSheet1_SLC2As as diagnostic markers and therapeutic targets in LUAD patients through bioinformatic analysis.docx（3.22 MB）

文件总体积 3.22 MB（源站 API 实测）。

数据说明

Facilitative glucose transporters (GLUTs), which are encoded by solute carrier 2A (SLC2A) genes, are responsible for mediating glucose absorption. In order to meet their higher energy demands, cancer cells are more likely than normal tissue cells to have elevated glucose transporters. Multiple pathogenic processes, such as cancer and immunological disorders, have been linked to GLUTs. Few studies, meanwhile, have been conducted on individuals with lung adenocarcinoma (LUAD) to evaluate all 14 SLC2A genes. We first identified increased protein levels of SLC2A1, SLC2A5, SLC2A6, and SLC2A9 via HPA database and downregulated mRNA levels of SLC2A3, SLC2A6, SLC2A9, and SLC2A14 by ONCOMINE and UALCAN databases in patients with LUAD. Additionally, lower levels of SLC2A3, SLC2A6, SLC2A9, SLC2A12, and SLC2A14 and higher levels of SLC2A1, SLC2A5, SLC2A10, and SLC2A11 had an association with advanced tumor stage. SLC2A1, SLC2A7, and SLC2A11 were identified as prognostic signatures for LUAD. Kaplan-Meier analysis, Univariate Cox regression, multivariate Cox regression and ROC analyses further revealed that these three genes signature was a novel and important prognostic factor. Mechanistically, the aberrant expression of these molecules was caused, in part, by the hypomethylation of SLC2A3, SLC2A10, and SLC2A14 and by the hypermethylation of SLC2A1, SLC2A2, SLC2A5, SLC2A6, SLC2A7, and SLC2A11. Additionally, SLC2A3, SLC2A5, SLC2A6, SLC2A9, and SLC2A14 contributed to LUAD by positively modulating M2 macrophage and T cell exhaustion. Finally, pathways involving SLC2A1/BUB1B/mitotic cell cycle, SLC2A5/CD86/negative regulation of immune system process, SLC2A6/PLEK/lymphocyte activation, SLC2A9/CD4/regulation of cytokine production might participate in the pathogenesis of LUAD. In summary, our results will provide the theoretical basis on SLC2As as diagnostic markers and therapeutic targets in LUAD.

许可

CC BY 4.0

引用

学术使用请引用 DOI 10.3389/fphar.2022.1045179.s001（source: https://frontiersin.figshare.com/articles/dataset/DataSheet1_SLC2As_as_diagnostic_markers_and_therapeutic_targets_in_LUAD_patients_through_bioinformatic_analysis_docx/21627524）。