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TCF19通过激活Raf/MEK/ERK信号通路促进肺癌细胞的增殖和肿瘤形成。

TCF19 promotes cell proliferation and tumor formation in lung cancer by activating the Raf/MEK/ERK signaling pathway.

作者信息

Tian Yahui, Xin Shaowei, Wan Zitong, Dong Honghong, Liu Lu, Fan Zhenzhen, Li Tian, Peng Fujun, Xiong Yanlu, Han Yong

机构信息

Department of Thoracic Surgery, Air Force Medical Center, Air Force Medical University, 30 Fucheng Rd, Beijing 100142, China; School of Basic Medical Sciences, Shandong Second Medical University, Weifang, China.

Department of Thoracic Surgery, Air Force Medical Center, Air Force Medical University, 30 Fucheng Rd, Beijing 100142, China.

出版信息

Transl Oncol. 2024 Jul;45:101978. doi: 10.1016/j.tranon.2024.101978. Epub 2024 May 2.

DOI:10.1016/j.tranon.2024.101978
PMID:38701650
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11088346/
Abstract

OBJECTIVE

This study aimed to investigate TCF19's role in lung cancer development, specifically its involvement in the RAF/MEK/ERK signaling pathway.

METHODS

Lung cancer tissue analysis revealed significant TCF19 overexpression. In vitro experiments using A549 and Hop62 cells with TCF19 overexpression demonstrated enhanced cell growth. Transgenic mouse models confirmed TCF19's role in primary tumor development. Transcriptome sequencing identified altered gene expression profiles, linking TCF19 to RAF/MEK/ERK pathway activation. Functional assays elucidated underlying mechanisms, revealing increased phosphorylation of Raf1, MEK1/2, and ERK1/2. Inhibiting RAF1 or ERK through shRaf1 or ERK inhibitor reduced cell cycle-related proteins and inhibited TCF19-overexpressing cell growth.

RESULTS

TCF19 was identified as an oncogene in lung carcinoma, specifically impacting the RAF/MEK/ERK pathway. Elevated TCF19 levels in lung cancer suggest targeting TCF19 or its associated pathways as a promising strategy for disease management.

CONCLUSION

This study unveils TCF19's oncogenic role in lung cancer, emphasizing its modulation of the RAF/MEK/ERK pathway and presenting a potential therapeutic target for TCF19-overexpressing lung cancers.

摘要

目的

本研究旨在探讨TCF19在肺癌发生发展中的作用，特别是其在RAF/MEK/ERK信号通路中的参与情况。

方法

肺癌组织分析显示TCF19显著过表达。使用过表达TCF19的A549和Hop62细胞进行的体外实验表明细胞生长增强。转基因小鼠模型证实了TCF19在原发性肿瘤发生中的作用。转录组测序确定了基因表达谱的改变，将TCF19与RAF/MEK/ERK通路激活联系起来。功能分析阐明了潜在机制，揭示了Raf1、MEK1/2和ERK1/2磷酸化增加。通过shRaf1或ERK抑制剂抑制RAF1或ERK可减少细胞周期相关蛋白并抑制过表达TCF19的细胞生长。

结果

TCF19被确定为肺癌中的一种致癌基因，特别是影响RAF/MEK/ERK通路。肺癌中TCF19水平升高表明靶向TCF19或其相关通路是一种有前景的疾病管理策略。

结论

本研究揭示了TCF19在肺癌中的致癌作用，强调了其对RAF/MEK/ERK通路的调节作用，并为过表达TCF19的肺癌提供了一个潜在的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/294f/11088346/7ee6d61afe99/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/294f/11088346/667985cd977e/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/294f/11088346/0dc1c41a971e/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/294f/11088346/2d016b9e6b7f/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/294f/11088346/d32c92bdce5c/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/294f/11088346/fded48a0c944/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/294f/11088346/febe4aafff6b/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/294f/11088346/7ee6d61afe99/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/294f/11088346/667985cd977e/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/294f/11088346/0dc1c41a971e/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/294f/11088346/2d016b9e6b7f/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/294f/11088346/d32c92bdce5c/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/294f/11088346/fded48a0c944/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/294f/11088346/febe4aafff6b/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/294f/11088346/7ee6d61afe99/gr6.jpg

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