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Btk 过表达抑制非小细胞肺癌细胞的增殖、迁移和侵袭。

Overexpression of Bruton Tyrosine Kinase Inhibits the Proliferation, Migration, and Invasion of Non-Small Cell Lung Cancer Cells.

机构信息

Department of Biotechnology, College of Life Science and Chemistry, Beijing University of Technology, Chaoyang, Beijing, China.

NHC Key Laboratory of biosafety, National Institute for Viral Disease Control and Prevention, Changping, Beijing, China.

出版信息

Anal Cell Pathol (Amst). 2023 Aug 18;2023:3377316. doi: 10.1155/2023/3377316. eCollection 2023.

DOI:10.1155/2023/3377316
PMID:37638060
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10457169/
Abstract

Lung cancer is one of the most lethal malignant tumors in the world. Non-small cell lung cancer (NSCLC) is the most common pathological subtype. However, the molecular mechanism of NSCLC progress is still unclear. We extracted the expression data of the Bruton's tyrosine kinase () gene in NSCLC tissues from the TCGA database. The results of paired -test showed that the gene was significantly underexpressed in NSCLC tissues. To further verify the above results, we detected the expression of the gene in NSCLC cell lines A549, H1299, and H1650 at the RNA and protein levels by real-time fluorescent quantitative polymerase chain reaction and Western Blot analysis, respectively. The results showed that BTK was low expressed in NSCLC tissues and cells. More importantly, the expression of the gene is also significantly related to the patient's age, gender, tumor range (T), lymph node invasion (N), tumor stage, and prognosis, and its expression level gradually decreases with the progress of the disease. It is speculated that BTK may be an independent prognostic factor of NSCLC. Our experimental results are consistent with the above clinical correlation analysis results. Overexpression of BTK can significantly inhibit the proliferation, migration, and invasion of NSCLC cells and can block the G0/G1 tumor cell cycle, indicating that overexpression of BTK can inhibit the growth, migration, and invasion of NSCLC cells.

摘要

肺癌是世界上最致命的恶性肿瘤之一。非小细胞肺癌(NSCLC)是最常见的病理亚型。然而,NSCLC 进展的分子机制仍不清楚。我们从 TCGA 数据库中提取了 NSCLC 组织中 Bruton 酪氨酸激酶(BTK)基因的表达数据。配对检验的结果表明,BTK 在 NSCLC 组织中显著低表达。为了进一步验证上述结果,我们通过实时荧光定量聚合酶链反应和 Western Blot 分析分别检测了 NSCLC 细胞系 A549、H1299 和 H1650 中 BTK 基因在 RNA 和蛋白质水平上的表达。结果表明,BTK 在 NSCLC 组织和细胞中低表达。更重要的是,BTK 基因的表达也与患者的年龄、性别、肿瘤范围(T)、淋巴结浸润(N)、肿瘤分期和预后显著相关,其表达水平随着疾病的进展逐渐降低。推测 BTK 可能是 NSCLC 的一个独立预后因素。我们的实验结果与上述临床相关性分析结果一致。BTK 的过表达可显著抑制 NSCLC 细胞的增殖、迁移和侵袭,并能阻断 G0/G1 肿瘤细胞周期,表明 BTK 的过表达能抑制 NSCLC 细胞的生长、迁移和侵袭。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bca1/10457169/404eab675ef5/ACP2023-3377316.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bca1/10457169/d6c889579b06/ACP2023-3377316.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bca1/10457169/45a917acc544/ACP2023-3377316.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bca1/10457169/976d8b0094a8/ACP2023-3377316.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bca1/10457169/c0410d56c0be/ACP2023-3377316.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bca1/10457169/404eab675ef5/ACP2023-3377316.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bca1/10457169/d6c889579b06/ACP2023-3377316.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bca1/10457169/45a917acc544/ACP2023-3377316.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bca1/10457169/976d8b0094a8/ACP2023-3377316.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bca1/10457169/c0410d56c0be/ACP2023-3377316.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bca1/10457169/404eab675ef5/ACP2023-3377316.005.jpg

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