Expression, immune infiltration, prognostic value, and clinical validation of RGS gene family in cancer: comprehensive analysis based on cellular metabolism.

IF 3.2 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM
Pengyu Chen, Bang Liu, Peiyao Wang, Zhaoxiong Zhang, Xin Liu, Shilong Li, Feng Zhu
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引用次数: 0

Abstract

Background: The regulator of G protein signalling (RGS) gene family is instrumental in tumour progression. However, the role of the RGS gene family in gastric cancer (GC) remains to be further elucidated.

Methods: A risk score model was constructed using least absolute shrinkage and selection operator (LASSO) regression, and nomogram integrating clinicopathological parameters was developed. Pathological information was collected from 115 patients with GC. Expression levels of relevant RGS genes were measured using absolute quantitative PCR to validate the accuracy of the model and nomogram.

Results: High expression of RGS1, RGS2, RGS4, and RGS5 correlated with shorter overall survival (OS). Five-gene risk models (RGS2, RGS3, RGS4, RGS5, and RGS16) effectively stratified patients into high- and low-risk groups, with patients in the high-risk group showing significantly shorter OS.

Conclusion: The RGS gene family is a prognostic biomarker and influences the immune microenvironment in GC. The developed risk model and nomogram are valuable personalised prognostic prediction.

RGS基因家族在肿瘤中的表达、免疫浸润、预后价值及临床验证:基于细胞代谢的综合分析
背景:G蛋白信号(RGS)基因家族的调节因子在肿瘤进展中起重要作用。然而,RGS基因家族在胃癌(GC)中的作用仍有待进一步阐明。方法:采用最小绝对收缩和选择算子(LASSO)回归建立风险评分模型,并综合临床病理参数建立nomogram。收集115例胃癌患者的病理资料。采用绝对定量PCR法检测相关RGS基因的表达水平,验证模型和图的准确性。结果:RGS1、RGS2、RGS4和RGS5高表达与总生存期(OS)缩短相关。五基因风险模型(RGS2、RGS3、RGS4、RGS5和RGS16)有效地将患者分为高危组和低危组,高危组患者的生存期明显缩短。结论:RGS基因家族是影响胃癌患者免疫微环境的预后生物标志物。所建立的风险模型和nomogram是一种有价值的个体化预后预测方法。
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来源期刊
Archives of Physiology and Biochemistry
Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY
CiteScore
6.90
自引率
3.30%
发文量
21
期刊介绍: Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.
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