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RPS27A在预后和免疫治疗中的潜在价值:从泛癌分析到肝细胞癌验证

The Potential Value of RPS27A in Prognosis and Immunotherapy: From Pan-Cancer Analysis to Hepatocellular Carcinoma Validation.

作者信息

Kuai Xingwang, Wei Chenyu, He Xiaoqian, Wang Fengli, Wang Chunbin, Ji Juling

机构信息

Department of Pathology, Medical School of Nantong University, Nantong, Jiangsu, 226000, People's Republic of China.

Department of Oncology, the Sixth Affiliated Hospital of Nantong University, Yanchen, Jiangsu, 224001, People's Republic of China.

出版信息

Immunotargets Ther. 2024 Dec 8;13:673-690. doi: 10.2147/ITT.S493217. eCollection 2024.

DOI:10.2147/ITT.S493217
PMID:39670220
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11636265/
Abstract

PURPOSE

Elucidation of the potential value of ribosomal protein S27a (RPS27A) for prognosis and immunotherapy in pan-cancer analysis, and exploration of the oncogenic function of RPS27A on hepatocellular carcinoma (HCC) and macrophage polarization.

METHODS

A systematic analysis of the function and mechanism of RPS27A was conducted with R software and multiple public platforms, including UALCAN, HPA, TISIDB, TIMER, cBioPortal, cancerSEA, TIDE, and TIMSO databases. The RPS27A expression in human and mouse liver was detected by immunohistochemistry. The biological behavior of HCC cells was detected in vitro after RPS27A overexpression. The influence of RPS27A on macrophage polarization was detected by the coculturing assay.

RESULTS

RPS27A dysregulation was found in multiple cancer types, and RPS27A level was associated with clinicopathologic features and prognosis in human cancers. RPS27A affected cancer statuses and multiple signaling pathways, such as DNA repair, invasion, IL10 synthesis, and MAPK activation. RPS27A took part in regulations of genomic alterations and heterogeneity and was associated with tumor mutation burden, microsatellite instability, neoantigen and so on. RPS27A expression was connected to the immune subtypes, tumor purity and immune cell infiltration and participated in regulation of the immunotherapy response. RPS27A was upregulated in HCC tissues compared to normal liver tissues. RPS27A overexpression in HCC cells promoted the proliferation, migration, and invasion of cancer cells, and accelerated M2 polarization of macrophage.

CONCLUSION

RPS27A had the potential to be a biomarker for diagnosis, prognosis and immunotherapy response in pan-cancer, and targeting RPS27A may provide new ideas for cancer immunotherapy.

摘要

目的

在泛癌分析中阐明核糖体蛋白S27a(RPS27A)对预后和免疫治疗的潜在价值,并探索RPS27A对肝细胞癌(HCC)的致癌功能及巨噬细胞极化的影响。

方法

使用R软件和多个公共平台,包括UALCAN、HPA、TISIDB、TIMER、cBioPortal、cancerSEA、TIDE和TIMSO数据库,对RPS27A的功能和机制进行系统分析。通过免疫组织化学检测人和小鼠肝脏中RPS27A的表达。RPS27A过表达后,在体外检测HCC细胞的生物学行为。通过共培养试验检测RPS27A对巨噬细胞极化的影响。

结果

在多种癌症类型中发现RPS27A失调,RPS27A水平与人类癌症的临床病理特征和预后相关。RPS27A影响癌症状态和多种信号通路,如DNA修复、侵袭、IL10合成和MAPK激活。RPS27A参与基因组改变和异质性的调控,并与肿瘤突变负荷、微卫星不稳定性、新抗原等相关。RPS27A表达与免疫亚型、肿瘤纯度和免疫细胞浸润有关,并参与免疫治疗反应的调节。与正常肝组织相比,RPS27A在HCC组织中上调。HCC细胞中RPS27A过表达促进癌细胞的增殖、迁移和侵袭,并加速巨噬细胞的M2极化。

结论

RPS27A有潜力成为泛癌诊断、预后和免疫治疗反应的生物标志物,靶向RPS27A可能为癌症免疫治疗提供新思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c932/11636265/cd65ae130830/ITT-13-673-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c932/11636265/0f3d2e9a6ebc/ITT-13-673-g0001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c932/11636265/8a526a22987a/ITT-13-673-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c932/11636265/0835cfa9ae52/ITT-13-673-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c932/11636265/6f406f8ffc9b/ITT-13-673-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c932/11636265/739c53082d35/ITT-13-673-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c932/11636265/cd65ae130830/ITT-13-673-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c932/11636265/0f3d2e9a6ebc/ITT-13-673-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c932/11636265/ad57189ab2d6/ITT-13-673-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c932/11636265/dafab2ce1dfe/ITT-13-673-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c932/11636265/8a526a22987a/ITT-13-673-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c932/11636265/0835cfa9ae52/ITT-13-673-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c932/11636265/6f406f8ffc9b/ITT-13-673-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c932/11636265/739c53082d35/ITT-13-673-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c932/11636265/cd65ae130830/ITT-13-673-g0008.jpg

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