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Results showed E6/E7 overexpression upregulated HDAC6 and DNMT3B and correlated with key cancer-related pathways, supported by qRT-PCR and Western blot. Findings suggest therapeutic target potential and a basis for further E6/E7 oncogenic mechanism 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was the study objective regarding HPV E6/E7 proteins?","Question",{"text":63,"@type":64},"To clarify how the HPV oncogenic proteins E6 and E7 regulate host processes, focusing on downstream gene changes relevant to HPV-related cervical cancer.","Answer",{"name":66,"@type":61,"acceptedAnswer":67},"How were recombinant adenoviruses prepared and used in the experiments?",{"text":68,"@type":64},"Recombinant adenoviral particles were constructed to express HPV16 and HPV18 E6/E7, then used to infect C33A cells to achieve sustained expression of E6/E7 before transcriptome analysis.",{"name":70,"@type":61,"acceptedAnswer":71},"Which genes and pathways were identified as upregulated after E6/E7 expression?",{"text":72,"@type":64},"RNA-Seq showed upregulation of HDAC6 and DNMT3B, and correlation analyses linked these genes to pathways including DNA replication, tumor proliferation signatures, G2M checkpoint, p53 pathways, and PI3K/AKT/mTOR 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10.3389/fcimb.2024.1459572  \nOPEN ACCESS  \nEDITED BY  \nShih-Heng Chen,  \nNational Institute of Environmental Health Sciences (NIH), United States  \nREVIEWED BY  \nNan Zheng,  \nNanjing University, China Irene Lo Cigno,  \nUniversity of Eastern Piedmont, Italy  \n*CORRESPONDENCE  \nJun Wang  \n[wj202fck@163.com](wj202fck@163.com)[ ](wj202fck@163.com)Peng Wang  \n [hellenhello@sina.com](hellenhello@sina.com)  \nRECEIVED 04 July 2024  \nACCEPTED 05 September 2024  \nPUBLISHED 01 October 2024  \nCITATION  \nShao Y, Shah PT, Su Q, Li S, Huang F, Wang J, Wang P and Wu C (2024) Recombinant adenoviruses expressing HPV16/18 E7  \nupregulate the HDAC6 and DNMT3B genes in C33A cells.  \nFront. Cell. Infect. Microbiol. 14:1459572 .  \ndoi: 10.3389/fcimb.2024.1459572  \nCOPYRIGHT  \n© 2024 Shao, Shah, Su, Li, Huang, Wang, Wang and Wu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) . The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.  \nRecombinant adenoviruses expressing HPV16/18 E7 upregulate the HDAC6 and DNMT3B genes in C33A cells  \nYunting Shao 1, Pir Tariq Shah 1, Qisheng Su 1, Shanhu Li 2, Fang Huang 2, Jun Wang 3*, Peng Wang 2* and Chengjun Wu 1  \n1 Faculty of Medicine, School of Basic Medical Sciences, Dalian University of Technology,  \nDalian, China, 2 Department of Cell Engineering, Beijing Institute of Biotechnology, Beijing, China,  \n3Obstetrics and Gynecology Department, The Second Affiliated Hospital of Dalian Medical University Mailing, Dalian, China  \nObjective: High-risk human papillomavirus (HPV) is a carcinogenic virus associated with nearly all cases of cervical cancer, as well as an increasing number of anal and oral cancers. The two carcinogenic proteins of HPV, E6 and E7, can immortalize keratinocytes and are essential for HPV-related cellular transformation. Currently, the global regulatory effects of these oncogenic proteins on the host proteome are not fully understood, and further exploration of the functions and carcinogenic mechanisms of E6 and E7 proteins is needed.  \nMethods: We used a previously established platform in our laboratory for constructing recombinant adenoviral plasmids expressing the HPV16 E7 gene to further construct recombinant virus particles expressing HPV16/18 E6, E7, and both E6 and E7 genes. These recombinant viruses were used to infect C33A cells to achieve sustained expression of the HPV16/18 E6/E7 genes. Subsequently, total RNA was extracted and RNA-Seq technology was employed fortranscriptome sequencing to identify differentially expressed genes associated with HPV infection in cervical cancer.  \nResults: RNA-Seq analysis revealed that overexpression of the HPV16/18 E6/E7 genes upregulated GP6, CD36, HDAC6, ESPL1, and DNMT3B among the differentially expressed genes (DEGs) associated with cervical cancer . Spearman correlation analysis revealed a statistically significant correlation between the HDAC6 and DNMT3B genes and key pathways, including DNA replication, tumor proliferation signature, G2M checkpoint, p53 pathways, and PI3K/AKT/mTOR signaling pathways. Further, qRT-PCR and Western blot analyses indicated that both HPV16/18 E7 can upregulate the expression of HDAC6 and DNMT3B, genes associated with HPV infection-related cervical cancer.  \nConclusion: The successful expression of HPV16/18 E6/E7 in cells indicates that the recombinant viruses retain the replication and infection capabilities of Ad4 . Furthermore, the recombinant viruses expressing HPV16/18 E7 can upregulate the HDAC6 and DNMT3B genes involved in cervical cancer pathways, thereby  \nFrontiers in Cellular and Infection Microbiology 01 [fronti","cbCaiiXFtqXR5SKI","https://ap.wps.com/l/cbCaiiXFtqXR5SKI","pdf",9627851,15,"English","# Introduction\n# Methods\n# Results\n# Conclusion","[{\"question\":\"What was the study objective regarding HPV E6/E7 proteins?\",\"answer\":\"To clarify how the HPV oncogenic proteins E6 and E7 regulate host processes, focusing on downstream gene changes relevant to HPV-related cervical cancer.\"},{\"question\":\"How were recombinant adenoviruses prepared and used in the experiments?\",\"answer\":\"Recombinant adenoviral particles were constructed to express HPV16 and HPV18 E6/E7, then used to infect C33A cells to achieve sustained expression of E6/E7 before transcriptome analysis.\"},{\"question\":\"Which genes and pathways were identified as upregulated after E6/E7 expression?\",\"answer\":\"RNA-Seq showed upregulation of HDAC6 and DNMT3B, and correlation analyses linked these genes to pathways including DNA replication, tumor proliferation signatures, G2M checkpoint, p53 pathways, and PI3K/AKT/mTOR signaling.\"}]","Recombinant adenoviruses expressing HPV16/18 E7 - upregulate the HDAC6 and DNMT3B genes in C33A cells | PDF",1789993162,38]