Dai Ya-Jie, Tang Hao-Dong, Jiang Guang-Qing, Xu Zhai-Yue
Department of General Surgery, Zhongda Hospital, Southeast University, Nanjing, Jiangsu 210009, PR China; Department of Surgery, School of Medicine, Southeast University, Nanjing, Jiangsu 210009, PR China.
Department of General Surgery, Zhongda Hospital, Southeast University, Nanjing, Jiangsu 210009, PR China; Department of Surgery, School of Medicine, Southeast University, Nanjing, Jiangsu 210009, PR China.
Transl Oncol. 2024 Nov;49:102110. doi: 10.1016/j.tranon.2024.102110. Epub 2024 Aug 24.
This study aims to identify key regulators of paraptosis in gastric cancer (GC) and explore their potential in guiding therapeutic strategies, especially in stomach adenocarcinoma (STAD). Genes associated with paraptosis were identified from the references and subjected to Cox regression analysis in the TCGA-STAD cohort. Using machine learning models, LPAR1 consistently ranked highest in feature importance. Multiple sequencing data showed that LPAR1 was significantly overexpressed in cancer-associated fibroblasts (CAFs). LPAR1 expression was significantly higher in normal tissues, and ROC analysis demonstrated its discriminative ability. Copy number alterations and microsatellite instability were significantly associated with LPAR1 expression. High LPAR1 expression correlated with advanced tumor grades and specific cancer immune subtypes, and multivariate analysis confirmed LPAR1 as an independent predictor of poor prognosis. LPAR1 expression was associated with different immune response metrics, including immune effector activation and upregulated chemokine secretion. High LPAR1 expression also correlated with increased sensitivity to compounds, such as BET bromodomain inhibitors I-BET151 and RITA, suggesting LPAR1 as a biomarker for predicting drug activity. FOXP2 showed a strong positive correlation with LPAR1 transcriptional regulation, while increased methylation of LPAR1 promoter regions was negatively correlated with gene expression. Knockdown of LPAR1 affected cell growth in most tumor cell lines, and in vitro experiments demonstrated that LPAR1 influenced extracellular matrix (ECM) contraction and cell viability in the paraptosis of CAFs. These findings suggest that LPAR1 is a critical regulator of paraptosis in GC and a potential biomarker for drug sensitivity and immunotherapy response. This underscores the role of CAFs in mediating tumorigenic effects and suggests that targeting LPAR1 could be a promising strategy for precision medicine in GC.
本研究旨在确定胃癌(GC)中副凋亡的关键调节因子,并探索其在指导治疗策略方面的潜力,尤其是在胃腺癌(STAD)中。从参考文献中鉴定出与副凋亡相关的基因,并在TCGA-STAD队列中进行Cox回归分析。使用机器学习模型,LPAR1在特征重要性方面始终排名最高。多项测序数据显示,LPAR1在癌症相关成纤维细胞(CAF)中显著过表达。LPAR1在正常组织中的表达显著更高,ROC分析证明了其判别能力。拷贝数改变和微卫星不稳定性与LPAR1表达显著相关。高LPAR1表达与肿瘤高级别和特定的癌症免疫亚型相关,多变量分析证实LPAR1是预后不良的独立预测因子。LPAR1表达与不同的免疫反应指标相关,包括免疫效应器激活和趋化因子分泌上调。高LPAR1表达还与对化合物(如BET溴结构域抑制剂I-BET151和RITA)的敏感性增加相关,表明LPAR1可作为预测药物活性的生物标志物。FOXP2与LPAR1转录调控呈强正相关,而LPAR1启动子区域甲基化增加与基因表达呈负相关。敲低LPAR1影响大多数肿瘤细胞系中的细胞生长,体外实验表明LPAR1在CAF的副凋亡中影响细胞外基质(ECM)收缩和细胞活力。这些发现表明,LPAR1是GC中副凋亡的关键调节因子,也是药物敏感性和免疫治疗反应的潜在生物标志物。这突出了CAF在介导致瘤效应中的作用,并表明靶向LPAR1可能是GC精准医学的一种有前景的策略。