Transcriptomic analysis reveals transcription factors implicated in radon-induced lung carcinogenesis.

IF 2.2 4区医学 Q3 TOXICOLOGY Toxicology Research Pub Date : 2024-10-03 eCollection Date: 2024-10-01 DOI:10.1093/toxres/tfae161

Xing Liu, Yuting Peng, Ruobing Chen, Yueyue Zhou, Xihuan Zou, Mingzhu Xia, Xinyi Wu, Meng Yu

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Abstract

Background: Radon, a potent carcinogen, is a significant catalyst for lung cancer development. However, the molecular mechanisms triggering radon-induced lung cancer remain elusive.

Methods: Utilizing a radon exposure concentration of 20,000 Bq/m3 for 20 min/session, malignant transformation was induced in human bronchial epithelial cells (BEAS-2B).

Results: Radon-exposed cells derived from passage 25 (BEAS-2B-Rn) exhibited enhanced proliferation and increased colony formation. Analysis of differential gene expression (DEG) through transcription factors revealed 663 up-regulated and 894 down-regulated genes in radon-exposed cells. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses revealed significant alterations in the malignant transformation pathway of cells, including those related to cancer and the PI3K/AKT signaling pathway. A PPI network analysis indicated a significant association of oncogenes, such as CCND1, KIT, and GATA3, with lung cancer among differentially expressed genes. In addition, the stability of the housekeeping gene was determined through RT-qPCR analysis, which also confirmed the results of transcriptome analysis.

Conclusions: The results suggest that transcription factors may play a pivotal role in conferring a survival advantage to radon-exposed cells. This is achieved by malignant transformation of human bronchial epithelial cells into lung carcinogenesis cell phenotypes.

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转录组分析揭示了与氡诱发肺癌有关的转录因子。

背景：氡是一种强致癌物质，是肺癌发生的重要催化剂。然而，诱发氡诱发肺癌的分子机制仍然难以捉摸：方法：利用 20,000 Bq/m3 的氡照射浓度，20 分钟/次，诱导人支气管上皮细胞（BEAS-2B）发生恶性转化：结果：氡暴露的第 25 期细胞（BEAS-2B-Rn）表现出增殖增强和集落形成增加。通过转录因子分析差异基因表达（DEG）发现，氡暴露细胞中有 663 个基因上调，894 个基因下调。基因本体（GO）和京都基因与基因组百科全书（KEGG）分析显示，细胞的恶性转化途径发生了显著改变，包括与癌症和 PI3K/AKT 信号途径相关的改变。PPI网络分析表明，在差异表达基因中，CCND1、KIT和GATA3等致癌基因与肺癌有显著关联。此外，通过 RT-qPCR 分析确定了看家基因的稳定性，这也证实了转录组分析的结果：结论：研究结果表明，转录因子在赋予暴露于氡的细胞生存优势方面可能起着关键作用。结论：研究结果表明，转录因子在赋予氡暴露细胞生存优势方面可能起着关键作用，而这是通过人类支气管上皮细胞向肺癌细胞表型的恶性转化实现的。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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