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布鲁顿酪氨酸激酶(BTK)敲低对肺腺癌生长及免疫反应的影响。

The impact of BTK knockdown on lung adenocarcinoma growth and immune response.

作者信息

Huang Jilan, Yuan Yufan, Guo Linghong, Xia Guojin, Chen Yan, Chen Qi, Wang Min

机构信息

Department of Radiology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.

Jiangxi Province Medical Imaging Research Institute, Nanchang, China.

出版信息

Cancer Sci. 2025 Jun;116(6):1550-1564. doi: 10.1111/cas.16394. Epub 2024 Dec 4.

Abstract

This study explores the molecular role of the BTK gene in lung adenocarcinoma (LUAD) progression and patient prognosis. Using a radiomics model based on BTK expression and PET-CT data analyzed through DeeplabV3, alongside transcriptomic and clinical data from TCGA, we established a strong predictive relationship between BTK levels and LUAD outcomes. Our findings demonstrate that low BTK expression is linked to poorer prognoses. Experimental models, including cell lines and in vivo mouse studies, revealed that BTK deficiency leads to increased LUAD cell proliferation, invasion, and metastasis. Furthermore, in vivo models indicated that BTK knockdown results in enhanced tumor growth and diminished CD8+ T cell activity. These results suggest that BTK plays a crucial role in modulating LUAD progression and the tumor immune environment, highlighting its potential as a therapeutic target.

摘要

本研究探讨了BTK基因在肺腺癌(LUAD)进展和患者预后中的分子作用。通过基于BTK表达和经DeeplabV3分析的PET-CT数据的放射组学模型,结合来自TCGA的转录组学和临床数据,我们建立了BTK水平与LUAD预后之间的强预测关系。我们的研究结果表明,低BTK表达与较差的预后相关。包括细胞系和体内小鼠研究在内的实验模型表明,BTK缺陷导致LUAD细胞增殖、侵袭和转移增加。此外,体内模型表明,BTK敲低导致肿瘤生长增强和CD8+T细胞活性降低。这些结果表明,BTK在调节LUAD进展和肿瘤免疫环境中起关键作用,突出了其作为治疗靶点的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0738/12127088/760e19dfeb2c/CAS-116-1550-g003.jpg

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