• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

口腔-肠道-肺部轴中微生物群与癌症相关细胞相互作用的全局转录组网络分析。

Global transcriptomic network analysis of the crosstalk between microbiota and cancer-related cells in the oral-gut-lung axis.

机构信息

Grupo de Investigación INPAC, Unidad de Investigación, Fundación Universitaria Sanitas, Bogotá, Colombia.

Dirección Académica, Universidad Nacional de Colombia, Sede de La Paz, La Paz, Colombia.

出版信息

Front Cell Infect Microbiol. 2024 Aug 20;14:1425388. doi: 10.3389/fcimb.2024.1425388. eCollection 2024.

DOI:10.3389/fcimb.2024.1425388
PMID:39228892
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11368877/
Abstract

BACKGROUND

The diagnosis and treatment of lung, colon, and gastric cancer through the histologic characteristics and genomic biomarkers have not had a strong impact on the mortality rates of the top three global causes of death by cancer.

METHODS

Twenty-five transcriptomic analyses (10 lung cancer, 10 gastric cancer, and 5 colon cancer datasets) followed our own bioinformatic pipeline based on the utilization of specialized libraries from the R language and DAVID´s gene enrichment analyses to identify a regulatory metafirm network of transcription factors and target genes common in every type of cancer, with experimental evidence that supports its relationship with the unlocking of cell phenotypic plasticity for the acquisition of the hallmarks of cancer during the tumoral process. The network's regulatory functional and signaling pathways might depend on the constant crosstalk with the microbiome network established in the oral-gut-lung axis.

RESULTS

The global transcriptomic network analysis highlighted the impact of transcription factors (SOX4, TCF3, TEAD4, ETV4, and FOXM1) that might be related to stem cell programming and cancer progression through the regulation of the expression of genes, such as cancer-cell membrane receptors, that interact with several microorganisms, including human T-cell leukemia virus 1 (HTLV-1), the human papilloma virus (HPV), the Epstein-Barr virus (EBV), and SARS-CoV-2. These interactions can trigger the MAPK, non-canonical WNT, and IFN signaling pathways, which regulate key transcription factor overexpression during the establishment and progression of lung, colon, and gastric cancer, respectively, along with the formation of the microbiome network.

CONCLUSION

The global transcriptomic network analysis highlights the important interaction between key transcription factors in lung, colon, and gastric cancer, which regulates the expression of cancer-cell membrane receptors for the interaction with the microbiome network during the tumorigenic process.

摘要

背景

通过组织学特征和基因组生物标志物对肺癌、结肠癌和胃癌进行诊断和治疗,并未对癌症导致的全球三大主要死亡原因的死亡率产生重大影响。

方法

我们采用了自己的生物信息学分析流程,对 25 项转录组分析(10 项肺癌数据集、10 项胃癌数据集和 5 项结肠癌数据集)进行了分析,这些分析均基于 R 语言的专用库的利用和 DAVID 的基因富集分析,以确定转录因子和靶基因的调控元网络,该网络在每一种癌症中都普遍存在,并且有实验证据支持其与细胞表型可塑性的解锁之间的关系,这种解锁是肿瘤发生过程中获得癌症标志性特征所必需的。该网络的调控功能和信号通路可能依赖于在口腔-肠道-肺部轴中建立的微生物组网络的持续串扰。

结果

全球转录组网络分析强调了转录因子(SOX4、TCF3、TEAD4、ETV4 和 FOXM1)的影响,这些转录因子可能通过调节与多种微生物相互作用的癌细胞膜受体的表达,与干细胞编程和癌症进展有关,这些微生物包括人类 T 细胞白血病病毒 1(HTLV-1)、人乳头瘤病毒(HPV)、爱泼斯坦-巴尔病毒(EBV)和 SARS-CoV-2。这些相互作用可以触发 MAPK、非经典 WNT 和 IFN 信号通路,分别调节肺癌、结肠癌和胃癌建立和进展过程中关键转录因子的过度表达,同时形成微生物组网络。

结论

全球转录组网络分析强调了肺癌、结肠癌和胃癌中关键转录因子之间的重要相互作用,这些相互作用调节了癌细胞膜受体的表达,以便在肿瘤发生过程中与微生物组网络相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d354/11368877/10c86635f0a8/fcimb-14-1425388-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d354/11368877/f17ed75c7730/fcimb-14-1425388-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d354/11368877/d57372014572/fcimb-14-1425388-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d354/11368877/b0c0a63706ef/fcimb-14-1425388-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d354/11368877/9909f32df16d/fcimb-14-1425388-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d354/11368877/26f9e844f92e/fcimb-14-1425388-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d354/11368877/101c8a3f183e/fcimb-14-1425388-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d354/11368877/b21cabf35254/fcimb-14-1425388-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d354/11368877/10c86635f0a8/fcimb-14-1425388-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d354/11368877/f17ed75c7730/fcimb-14-1425388-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d354/11368877/d57372014572/fcimb-14-1425388-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d354/11368877/b0c0a63706ef/fcimb-14-1425388-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d354/11368877/9909f32df16d/fcimb-14-1425388-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d354/11368877/26f9e844f92e/fcimb-14-1425388-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d354/11368877/101c8a3f183e/fcimb-14-1425388-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d354/11368877/b21cabf35254/fcimb-14-1425388-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d354/11368877/10c86635f0a8/fcimb-14-1425388-g008.jpg

相似文献

1
Global transcriptomic network analysis of the crosstalk between microbiota and cancer-related cells in the oral-gut-lung axis.口腔-肠道-肺部轴中微生物群与癌症相关细胞相互作用的全局转录组网络分析。
Front Cell Infect Microbiol. 2024 Aug 20;14:1425388. doi: 10.3389/fcimb.2024.1425388. eCollection 2024.
2
Host Transcriptional Regulatory Genes and Microbiome Networks Crosstalk through Immune Receptors Establishing Normal and Tumor Multiomics Metafirm of the Oral-Gut-Lung Axis.宿主转录调控基因与微生物组网络通过免疫受体相互作用,建立口腔-肠道-肺部轴的正常和肿瘤多组学元模型。
Int J Mol Sci. 2023 Nov 23;24(23):16638. doi: 10.3390/ijms242316638.
3
Network Analysis of Gut Microbiome and Metabolome to Discover Microbiota-Linked Biomarkers in Patients Affected by Non-Small Cell Lung Cancer.基于肠道微生物组和代谢组的网络分析发现非小细胞肺癌患者相关的微生物组生物标志物。
Int J Mol Sci. 2020 Nov 19;21(22):8730. doi: 10.3390/ijms21228730.
4
Identifying General Tumor and Specific Lung Cancer Biomarkers by Transcriptomic Analysis.通过转录组分析鉴定通用肿瘤和特定肺癌生物标志物
Biology (Basel). 2022 Jul 20;11(7):1082. doi: 10.3390/biology11071082.
5
Human non-small cell lung cancer expresses putative cancer stem cell markers and exhibits the transcriptomic profile of multipotent cells.人类非小细胞肺癌表达假定的癌症干细胞标志物,并表现出多能细胞的转录组特征。
BMC Cancer. 2015 Feb 25;15:84. doi: 10.1186/s12885-015-1086-3.
6
Large differences in global transcriptional regulatory programs of normal and tumor colon cells.正常结肠细胞与肿瘤结肠细胞的全球转录调控程序存在巨大差异。
BMC Cancer. 2014 Sep 24;14:708. doi: 10.1186/1471-2407-14-708.
7
Regulatory mechanisms of transcription factors and target genes on gastric cancer by bioinformatics method.基于生物信息学方法的转录因子与靶基因对胃癌的调控机制
Hepatogastroenterology. 2015 Mar-Apr;62(138):524-8.
8
SNHG8 is identified as a key regulator of epstein-barr virus(EBV)-associated gastric cancer by an integrative analysis of lncRNA and mRNA expression.通过lncRNA和mRNA表达的综合分析,SNHG8被鉴定为与爱泼斯坦-巴尔病毒(EBV)相关的胃癌的关键调节因子。
Oncotarget. 2016 Dec 6;7(49):80990-81002. doi: 10.18632/oncotarget.13167.
9
Possible Molecular Mechanisms for the Roles of MicroRNA-21 Played in Lung Cancer.miR-21 在肺癌中作用的可能分子机制
Technol Cancer Res Treat. 2019 Jan 1;18:1533033819875130. doi: 10.1177/1533033819875130.
10
Lung Cancer Gene Regulatory Network of Transcription Factors Related to the Hallmarks of Cancer.与癌症特征相关的转录因子的肺癌基因调控网络
Curr Issues Mol Biol. 2023 Jan 5;45(1):434-464. doi: 10.3390/cimb45010029.

引用本文的文献

1
Interplay of Transcriptomic Regulation, Microbiota, and Signaling Pathways in Lung and Gut Inflammation-Induced Tumorigenesis.肺和肠道炎症诱导肿瘤发生过程中转录组调控、微生物群与信号通路的相互作用
Cells. 2024 Dec 24;14(1):1. doi: 10.3390/cells14010001.

本文引用的文献

1
Recent advances in molecular targeted therapy of lung cancer: Possible application in translation medicine.肺癌分子靶向治疗的最新进展:在转化医学中的可能应用。
Iran J Basic Med Sci. 2024;27(2):122-133. doi: 10.22038/IJBMS.2023.72407.15749.
2
Roles of epidermal growth factor receptor, claudin-1 and occludin in multi-step entry of hepatitis C virus into polarized hepatoma spheroids.表皮生长因子受体、紧密连接蛋白-1 和闭合蛋白在丙型肝炎病毒进入极化肝癌球体的多步进入中的作用。
PLoS Pathog. 2023 Dec 29;19(12):e1011887. doi: 10.1371/journal.ppat.1011887. eCollection 2023 Dec.
3
TEAD4: A key regulator of tumor metastasis and chemoresistance - Mechanisms and therapeutic implications.
TEAD4:肿瘤转移和化疗耐药的关键调节因子——机制与治疗意义。
Biochim Biophys Acta Rev Cancer. 2024 Jan;1879(1):189050. doi: 10.1016/j.bbcan.2023.189050. Epub 2023 Dec 8.
4
Host Transcriptional Regulatory Genes and Microbiome Networks Crosstalk through Immune Receptors Establishing Normal and Tumor Multiomics Metafirm of the Oral-Gut-Lung Axis.宿主转录调控基因与微生物组网络通过免疫受体相互作用,建立口腔-肠道-肺部轴的正常和肿瘤多组学元模型。
Int J Mol Sci. 2023 Nov 23;24(23):16638. doi: 10.3390/ijms242316638.
5
Global variations in lung cancer incidence by histological subtype in 2020: a population-based study.2020 年按组织学亚型划分的全球肺癌发病率变化:一项基于人群的研究。
Lancet Oncol. 2023 Nov;24(11):1206-1218. doi: 10.1016/S1470-2045(23)00444-8. Epub 2023 Oct 11.
6
Transcription factor TEAD4 facilitates glycolysis and proliferation of gastric cancer cells by activating PKMYT1.转录因子 TEAD4 通过激活 PKMYT1 促进胃癌细胞的糖酵解和增殖。
Mol Cell Probes. 2023 Dec;72:101932. doi: 10.1016/j.mcp.2023.101932. Epub 2023 Nov 2.
7
Transcription factor ETV4 promotes the development of hepatocellular carcinoma by driving hepatic TNF-α signaling.转录因子 ETV4 通过驱动肝组织 TNF-α 信号通路促进肝癌的发展。
Cancer Commun (Lond). 2023 Dec;43(12):1354-1372. doi: 10.1002/cac2.12482. Epub 2023 Sep 5.
8
The Effect of GLUT1 and HIF-1α Expressions on Glucose Uptake and Patient Survival in Non-Small-Cell Lung Carcinoma.GLUT1 和 HIF-1α 表达对非小细胞肺癌葡萄糖摄取和患者生存的影响。
Int J Mol Sci. 2023 Jun 24;24(13):10575. doi: 10.3390/ijms241310575.
9
Variations in Genes Encoding Human Papillomavirus Binding Receptors and Susceptibility to Cervical Precancer.HPV 结合受体编码基因的变异与宫颈癌前病变易感性的关系。
Cancer Epidemiol Biomarkers Prev. 2023 Sep 1;32(9):1190-1197. doi: 10.1158/1055-9965.EPI-23-0300.
10
γ-tocotrienol regulates gastric cancer by targeting notch signaling pathway.γ-生育三烯酚通过靶向 Notch 信号通路调控胃癌。
Hereditas. 2023 Apr 13;160(1):15. doi: 10.1186/s41065-023-00277-w.