| 李润之,林鹏,陈圣乐,等.肺腺癌关键致癌驱动因子LRFN3的多组学分析研究（英文）[J].中国海洋药物,2027,(2):-. |
| 肺腺癌关键致癌驱动因子LRFN3的多组学分析研究（英文） |
| Multi-omics analysis of LRFN3 as a key oncogenic driver in lung adenocarcinoma |
| 投稿时间：2026-02-04 修订日期：2026-03-15 |
| DOI： |
| 中文关键词: LRFN3 泛癌 JAK-STAT信号通路 预后生物标志物 |
| English Keywords:LRFN3 pan-cancer JAK-STAT signaling prognostic biomarker |
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| 中文摘要: |
| 目的 研究LRFN3在癌症进展中的作用，并评估其作为治疗靶点的潜力。方法 首先通过系统性泛癌生物信息学分析，阐明了LRFN3在不同肿瘤中的表达模式、突变特征、预后价值及其基因组关联，随后在肺癌模型中开展实验验证，以揭示LRFN3的致癌功能及其相关分子机制。结果 生物信息学分析结果显示，LRFN3在多种肿瘤中显著上调，其中在肺腺癌（LUAD）中上调频率最高、幅度最为显著。LRFN3表达升高及其高频突变与患者不良预后、基因组不稳定性及侵袭性临床病理特征相关。临床分析证实，在肺腺癌中，LRFN3的表达水平与肿瘤分期、解剖部位及吸烟史显著相关。机制预测表明，LRFN3的异常表达可能通过转录下调PTPRD/PTPRS，导致JAK-STAT信号通路过度激活。实验验证证实，LRFN3在肺腺癌组织及已建立的肺腺癌细胞系中均存在过表达。敲低LRFN3能显著抑制肺腺癌细胞的增殖、迁移及侵袭能力，并减弱JAK-STAT信号通路的激活。结论 LRFN3在肿瘤（尤其是肺腺癌）的恶性进展中发挥关键作用，这使其成为一个极具前景的治疗靶点与预后生物标志物，为开发靶向LRFN3的治疗策略提供了依据。 |
| English Summary: |
| Objective To study the role of LRFN3 in cancer progression and evaluate its potential as a therapeutic target. Methods A comprehensive pan-cancer bioinformatic analysis was performed to characterize the expression, mutation, prognostic relevance, and genomic associations of LRFN3 across tumor types, followed by experimental validation of its oncogenic function and associated molecular mechanisms in lung cancer models. Results Bioinformatics analysis revealed that LRFN3 was significantly upregulated in multiple tumors, with the most frequency and magnitude observed in Lung Adenocarcinoma (LUAD). Elevated LRFN3 expression and recurrent mutations were correlated with poor prognosis, genomic instability and aggressive clinicopathological features. Clinically, LRFN3 expression was confirmed to correlate significantly with tumor stage, anatomical location, smoking history in LUAD. Mechanistic prediction indicates that aberrant expression of LRFN3 was predicted to hyperactivate JAK-STAT signaling by transcriptional downregulation of PTPRD/PTPRS. Experimental validation confirmed consistent overexpression of LRFN3 in lung adenocarcinoma tissues and established LUAD cell lines. Knockdown of LRFN3 markedly suppressed proliferation, migration, and invasion of LUAD cells and attenuated the activation of the JAK-STAT pathway. Conclusion LRFN3 plays a pivotal role in the malignant progression of tumors, particularly in LUAD, positioning it as a promising therapeutic target and prognostic biomarker for the development of LRFN3-targeted therapies. |
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