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SLC7A11,肺腺癌的潜在免疫治疗靶点。

SLC7A11, a potential immunotherapeutic target in lung adenocarcinoma.

机构信息

Department of Respiration, Chengdu First People's Hospital, No. 18, Wangxiang North Road, High-Tech Zone, Chengdu, 610041, Sichuan Province, People's Republic of China.

出版信息

Sci Rep. 2023 Oct 25;13(1):18302. doi: 10.1038/s41598-023-45284-z.

DOI:10.1038/s41598-023-45284-z
PMID:37880315
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10600206/
Abstract

SLC7A11 has significant translational value in cancer treatment. However, there are few studies on whether SLC7A11 affects the immune status of lung adenocarcinoma (LUAD). Information on SLC7A11 expression and its impact on prognosis was obtained from the cancer genome atlas and gene expression omnibus databases. The differentially expressed genes (DEGs) were analysed by GO and KEGG. GSEA enrichment analysis was performed in the SLC7A11-high and SLC7A11-low groups. The relationship between SLC7A11 and tumour immunity, immune checkpoints, and immune cell infiltration was studied using R language. We analysed the correlation between SLC7A11 and chemotactic factors (CFs) and chemokine receptors using the TISIDB database. SLC7A11 is overexpressed in many tumours, including LUAD. The 5-year overall survival of patients in the SLC7A11-high group was lower than in the SLC7A11-low group. KEGG analysis found that the DEGs were enriched in ferroptosis signaling pathways. GSEA analysis found that the survival-related signaling pathways were enriched in the SLC7A11-low group. The SLC7A11-low group had higher immune scores and immune checkpoint expression. SLC7A11 was negatively correlated with many immune cells (CD8+ T cells, immature dendritic cells), CFs, chemokine receptors (such as CCL17/19/22/23, CXCL9/10/11/14, CCR4/6, CX3CR1, CXCR3) and MHCs (major histocompatibility complex). SLC7A11 may regulate tumour immunity and could be a potential therapeutic target for LUAD.

摘要

SLC7A11 在癌症治疗中具有重要的翻译价值。然而,关于 SLC7A11 是否影响肺腺癌(LUAD)的免疫状态的研究较少。从癌症基因组图谱和基因表达综合数据库中获取 SLC7A11 表达及其对预后影响的信息。通过 GO 和 KEGG 分析差异表达基因(DEGs)。在 SLC7A11 高表达和 SLC7A11 低表达组中进行 GSEA 富集分析。使用 R 语言研究 SLC7A11 与肿瘤免疫、免疫检查点和免疫细胞浸润的关系。使用 TISIDB 数据库分析 SLC7A11 与趋化因子(CFs)和趋化因子受体的相关性。SLC7A11 在许多肿瘤中过表达,包括 LUAD。SLC7A11 高表达组患者的 5 年总生存率低于 SLC7A11 低表达组。KEGG 分析发现,DEGs 富集在铁死亡信号通路中。GSEA 分析发现,SLC7A11 低表达组中与生存相关的信号通路富集。SLC7A11 低表达组的免疫评分和免疫检查点表达较高。SLC7A11 与许多免疫细胞(CD8+T 细胞、未成熟树突状细胞)、CFs、趋化因子受体(如 CCL17/19/22/23、CXCL9/10/11/14、CCR4/6、CX3CR1、CXCR3)和 MHCs(主要组织相容性复合体)呈负相关。SLC7A11 可能调节肿瘤免疫,可能是 LUAD 的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c662/10600206/9f114f1fae68/41598_2023_45284_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c662/10600206/d69f4922f8f0/41598_2023_45284_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c662/10600206/4520e4c84a33/41598_2023_45284_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c662/10600206/39c1b893da68/41598_2023_45284_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c662/10600206/38240e2e57de/41598_2023_45284_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c662/10600206/ffd7267ac920/41598_2023_45284_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c662/10600206/9f114f1fae68/41598_2023_45284_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c662/10600206/d69f4922f8f0/41598_2023_45284_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c662/10600206/4520e4c84a33/41598_2023_45284_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c662/10600206/39c1b893da68/41598_2023_45284_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c662/10600206/38240e2e57de/41598_2023_45284_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c662/10600206/ffd7267ac920/41598_2023_45284_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c662/10600206/9f114f1fae68/41598_2023_45284_Fig6_HTML.jpg

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