A lactylation-related gene signature predicts prognosis and immunotherapy response in clear cell renal cell carcinoma based on machine learning and multi-omics analysis

基于机器学习和多组学分析的乳酸化相关基因特征可预测透明细胞肾细胞癌的预后和免疫治疗反应

阅读:1

Abstract

Clear cell renal cell carcinoma (ccRCC) is a highly heterogeneous malignancy with complex molecular features, posing significant challenges for accurate prognosis prediction and treatment stratification. Lactylation, an emerging epigenetic regulatory mechanism, plays a pivotal role in tumor progression and immune microenvironment remodeling. This study aims to develop a lactylation-related gene signature (LRGS) and systematically evaluate its prognostic value and potential for guiding clinical interventions in ccRCC. We developed a machine learning-derived lactylation signature using lactylation-related genes (LRGs) selected through bulk and single-cell RNA sequencing data. The model’s performance was subsequently validated using internal (TCGA-KIRC) and external (E-MTAB-1980) cohorts. The associations of LRGS with clinical characteristics, immune cell infiltration, and drug response were further analyzed. The functions of the key risk gene SHC1 were investigated using in vitro experiments. Ultimately, an 11-gene LRGS was identified that effectively predicts the prognosis of ccRCC patients. This model demonstrated robust predictive capability in an external dataset (AUC > 0.7). Univariate and multivariate analyses indicated that the model’s risk score was an independent predictor of clinical outcomes. The high-risk group exhibited significant infiltration of Tregs and a higher tumor immune dysfunction score, indicating a poorer responsiveness to immunotherapy. Finally, cell experiments confirmed that inhibiting SHC1 expression suppressed the proliferation and migration of ccRCC cells. In conclusion, we successfully constructed a novel LRGS, which provides a new perspective for risk stratification and personalized treatment of ccRCC. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12672-026-04781-z.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。