Gene Expression Analysis of Human Papillomavirus-Associated Colorectal Carcinoma

Purpose. Human papillomavirus (HPV) antigens had been found in colorectal cancer (CRC) tissue, but little evidence demonstrates the association of HPV with oncogene mutations in CRC. We aim to elucidate the mutated genes that link HPV infection and CRC carcinogenesis. Methods. Cancerous and adjacent...

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Veröffentlicht in:BioMed research international 2020, Vol.2020 (2020), p.1-14
Hauptverfasser: Xie, Yanxuan, Liu, Kaixi, Chen, Xiang, Jiao, Xiaoyang, Chen, Jinghong, Yuan, Yumeng, Sun, Jiayu, Shen, Wenjun, Yao, Fen, Fan, Zhiqiang, Li, Yazhen, Qiu, Qiancheng, Cai, Leshan
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container_end_page 14
container_issue 2020
container_start_page 1
container_title BioMed research international
container_volume 2020
creator Xie, Yanxuan
Liu, Kaixi
Chen, Xiang
Jiao, Xiaoyang
Chen, Jinghong
Yuan, Yumeng
Sun, Jiayu
Shen, Wenjun
Yao, Fen
Fan, Zhiqiang
Li, Yazhen
Qiu, Qiancheng
Cai, Leshan
description Purpose. Human papillomavirus (HPV) antigens had been found in colorectal cancer (CRC) tissue, but little evidence demonstrates the association of HPV with oncogene mutations in CRC. We aim to elucidate the mutated genes that link HPV infection and CRC carcinogenesis. Methods. Cancerous and adjacent noncancerous tissues were obtained from CRC patients. HPV antigen was measured by using the immunohistochemical (IHC) technique. The differentially expressed genes (DEGs) in HPV-positive and HPV-negative tumor tissues were measured by using TaqMan Array Plates. The target genes were validated with the qPCR method. Results. 15 (31.9%) cases of CRC patients were observed to be HPV positive, in which HPV antigen was expressed in most tumor tissues rather than in adjacent noncancerous tissues. With TaqMan Array Plates analyses, we found that 39 differentially expressed genes (DEGs) were upregulated, while 17 DEGs were downregulated in HPV-positive CRC tissues compared with HPV-negative tissues. Four DEGs (MMP-7, MYC, WNT-5A, and AXIN2) were upregulated in tumor vs. normal tissues, or adenoma vs. normal tissue in TCGA, which was overlapped with our data. In the confirmation test, MMP-7, MYC, WNT-5A, and AXIN2 were upregulated in cancerous tissue compared with adjacent noncancerous tissue. MYC, WNT-5A, and AXIN2 were shown to be upregulated in HPV-positive CRC tissues when compared to HPV-negative tissues. Conclusion. HPV-encoding genome may integrate into the tumor genomes that involved in multiple signaling pathways. Further genomic and proteomic investigation is necessary for obtaining a more comprehensive knowledge of signaling pathways associated with the CRC carcinogenesis.
doi_str_mv 10.1155/2020/5201587
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Human papillomavirus (HPV) antigens had been found in colorectal cancer (CRC) tissue, but little evidence demonstrates the association of HPV with oncogene mutations in CRC. We aim to elucidate the mutated genes that link HPV infection and CRC carcinogenesis. Methods. Cancerous and adjacent noncancerous tissues were obtained from CRC patients. HPV antigen was measured by using the immunohistochemical (IHC) technique. The differentially expressed genes (DEGs) in HPV-positive and HPV-negative tumor tissues were measured by using TaqMan Array Plates. The target genes were validated with the qPCR method. Results. 15 (31.9%) cases of CRC patients were observed to be HPV positive, in which HPV antigen was expressed in most tumor tissues rather than in adjacent noncancerous tissues. With TaqMan Array Plates analyses, we found that 39 differentially expressed genes (DEGs) were upregulated, while 17 DEGs were downregulated in HPV-positive CRC tissues compared with HPV-negative tissues. Four DEGs (MMP-7, MYC, WNT-5A, and AXIN2) were upregulated in tumor vs. normal tissues, or adenoma vs. normal tissue in TCGA, which was overlapped with our data. In the confirmation test, MMP-7, MYC, WNT-5A, and AXIN2 were upregulated in cancerous tissue compared with adjacent noncancerous tissue. MYC, WNT-5A, and AXIN2 were shown to be upregulated in HPV-positive CRC tissues when compared to HPV-negative tissues. Conclusion. HPV-encoding genome may integrate into the tumor genomes that involved in multiple signaling pathways. Further genomic and proteomic investigation is necessary for obtaining a more comprehensive knowledge of signaling pathways associated with the CRC carcinogenesis.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2020/5201587</identifier><identifier>PMID: 32258125</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Adenoma ; Adult ; Aged ; Aged, 80 and over ; Antigens ; Arrays ; Bioinformatics ; Cancer ; Carcinogenesis ; Carcinogens ; Colorectal cancer ; Colorectal carcinoma ; Colorectal Neoplasms - metabolism ; Colorectal Neoplasms - pathology ; Colorectal Neoplasms - virology ; Deoxyribonucleic acid ; Development and progression ; DNA ; Ethics ; Female ; Gene expression ; Gene Expression Regulation, Neoplastic ; Gene mutations ; Genes ; Genetic aspects ; Genomes ; Genomics ; Health aspects ; Human papillomavirus ; Humans ; Infections ; Male ; Matrilysin ; Metastasis ; Middle Aged ; Mutation ; Myc protein ; Neoplasm Proteins - biosynthesis ; Papillomaviridae - metabolism ; Papillomavirus infections ; Papillomavirus Infections - metabolism ; Papillomavirus Infections - pathology ; Papillomaviruses ; Pathogenesis ; Patients ; Plates ; Proteomics ; Sample size ; Signal transduction ; Signaling ; Software ; Tissues ; Tumors ; Wnt protein</subject><ispartof>BioMed research international, 2020, Vol.2020 (2020), p.1-14</ispartof><rights>Copyright © 2020 Qiancheng Qiu et al.</rights><rights>COPYRIGHT 2020 John Wiley &amp; Sons, Inc.</rights><rights>Copyright © 2020 Qiancheng Qiu et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2020 Qiancheng Qiu et al. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-b8c12995b78d932b41e05fb1da2e71785bba2844de0868eccc4467c8a21e0f073</citedby><cites>FETCH-LOGICAL-c499t-b8c12995b78d932b41e05fb1da2e71785bba2844de0868eccc4467c8a21e0f073</cites><orcidid>0000-0002-7568-0595 ; 0000-0002-1764-4748</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7103040/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7103040/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,4021,27921,27922,27923,53789,53791</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32258125$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Maruyama, Satoshi</contributor><contributor>Satoshi Maruyama</contributor><creatorcontrib>Xie, Yanxuan</creatorcontrib><creatorcontrib>Liu, Kaixi</creatorcontrib><creatorcontrib>Chen, Xiang</creatorcontrib><creatorcontrib>Jiao, Xiaoyang</creatorcontrib><creatorcontrib>Chen, Jinghong</creatorcontrib><creatorcontrib>Yuan, Yumeng</creatorcontrib><creatorcontrib>Sun, Jiayu</creatorcontrib><creatorcontrib>Shen, Wenjun</creatorcontrib><creatorcontrib>Yao, Fen</creatorcontrib><creatorcontrib>Fan, Zhiqiang</creatorcontrib><creatorcontrib>Li, Yazhen</creatorcontrib><creatorcontrib>Qiu, Qiancheng</creatorcontrib><creatorcontrib>Cai, Leshan</creatorcontrib><title>Gene Expression Analysis of Human Papillomavirus-Associated Colorectal Carcinoma</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>Purpose. Human papillomavirus (HPV) antigens had been found in colorectal cancer (CRC) tissue, but little evidence demonstrates the association of HPV with oncogene mutations in CRC. We aim to elucidate the mutated genes that link HPV infection and CRC carcinogenesis. Methods. Cancerous and adjacent noncancerous tissues were obtained from CRC patients. HPV antigen was measured by using the immunohistochemical (IHC) technique. The differentially expressed genes (DEGs) in HPV-positive and HPV-negative tumor tissues were measured by using TaqMan Array Plates. The target genes were validated with the qPCR method. Results. 15 (31.9%) cases of CRC patients were observed to be HPV positive, in which HPV antigen was expressed in most tumor tissues rather than in adjacent noncancerous tissues. With TaqMan Array Plates analyses, we found that 39 differentially expressed genes (DEGs) were upregulated, while 17 DEGs were downregulated in HPV-positive CRC tissues compared with HPV-negative tissues. Four DEGs (MMP-7, MYC, WNT-5A, and AXIN2) were upregulated in tumor vs. normal tissues, or adenoma vs. normal tissue in TCGA, which was overlapped with our data. In the confirmation test, MMP-7, MYC, WNT-5A, and AXIN2 were upregulated in cancerous tissue compared with adjacent noncancerous tissue. MYC, WNT-5A, and AXIN2 were shown to be upregulated in HPV-positive CRC tissues when compared to HPV-negative tissues. Conclusion. HPV-encoding genome may integrate into the tumor genomes that involved in multiple signaling pathways. 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Liu, Kaixi ; Chen, Xiang ; Jiao, Xiaoyang ; Chen, Jinghong ; Yuan, Yumeng ; Sun, Jiayu ; Shen, Wenjun ; Yao, Fen ; Fan, Zhiqiang ; Li, Yazhen ; Qiu, Qiancheng ; Cai, Leshan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c499t-b8c12995b78d932b41e05fb1da2e71785bba2844de0868eccc4467c8a21e0f073</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Adenoma</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Antigens</topic><topic>Arrays</topic><topic>Bioinformatics</topic><topic>Cancer</topic><topic>Carcinogenesis</topic><topic>Carcinogens</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Colorectal Neoplasms - metabolism</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Colorectal Neoplasms - virology</topic><topic>Deoxyribonucleic acid</topic><topic>Development and progression</topic><topic>DNA</topic><topic>Ethics</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene mutations</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genomes</topic><topic>Genomics</topic><topic>Health aspects</topic><topic>Human papillomavirus</topic><topic>Humans</topic><topic>Infections</topic><topic>Male</topic><topic>Matrilysin</topic><topic>Metastasis</topic><topic>Middle Aged</topic><topic>Mutation</topic><topic>Myc protein</topic><topic>Neoplasm Proteins - biosynthesis</topic><topic>Papillomaviridae - metabolism</topic><topic>Papillomavirus infections</topic><topic>Papillomavirus Infections - metabolism</topic><topic>Papillomavirus Infections - pathology</topic><topic>Papillomaviruses</topic><topic>Pathogenesis</topic><topic>Patients</topic><topic>Plates</topic><topic>Proteomics</topic><topic>Sample size</topic><topic>Signal transduction</topic><topic>Signaling</topic><topic>Software</topic><topic>Tissues</topic><topic>Tumors</topic><topic>Wnt protein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xie, Yanxuan</creatorcontrib><creatorcontrib>Liu, Kaixi</creatorcontrib><creatorcontrib>Chen, Xiang</creatorcontrib><creatorcontrib>Jiao, Xiaoyang</creatorcontrib><creatorcontrib>Chen, Jinghong</creatorcontrib><creatorcontrib>Yuan, Yumeng</creatorcontrib><creatorcontrib>Sun, Jiayu</creatorcontrib><creatorcontrib>Shen, Wenjun</creatorcontrib><creatorcontrib>Yao, Fen</creatorcontrib><creatorcontrib>Fan, Zhiqiang</creatorcontrib><creatorcontrib>Li, Yazhen</creatorcontrib><creatorcontrib>Qiu, Qiancheng</creatorcontrib><creatorcontrib>Cai, Leshan</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic Complete</collection><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health &amp; 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Human papillomavirus (HPV) antigens had been found in colorectal cancer (CRC) tissue, but little evidence demonstrates the association of HPV with oncogene mutations in CRC. We aim to elucidate the mutated genes that link HPV infection and CRC carcinogenesis. Methods. Cancerous and adjacent noncancerous tissues were obtained from CRC patients. HPV antigen was measured by using the immunohistochemical (IHC) technique. The differentially expressed genes (DEGs) in HPV-positive and HPV-negative tumor tissues were measured by using TaqMan Array Plates. The target genes were validated with the qPCR method. Results. 15 (31.9%) cases of CRC patients were observed to be HPV positive, in which HPV antigen was expressed in most tumor tissues rather than in adjacent noncancerous tissues. With TaqMan Array Plates analyses, we found that 39 differentially expressed genes (DEGs) were upregulated, while 17 DEGs were downregulated in HPV-positive CRC tissues compared with HPV-negative tissues. Four DEGs (MMP-7, MYC, WNT-5A, and AXIN2) were upregulated in tumor vs. normal tissues, or adenoma vs. normal tissue in TCGA, which was overlapped with our data. In the confirmation test, MMP-7, MYC, WNT-5A, and AXIN2 were upregulated in cancerous tissue compared with adjacent noncancerous tissue. MYC, WNT-5A, and AXIN2 were shown to be upregulated in HPV-positive CRC tissues when compared to HPV-negative tissues. Conclusion. HPV-encoding genome may integrate into the tumor genomes that involved in multiple signaling pathways. Further genomic and proteomic investigation is necessary for obtaining a more comprehensive knowledge of signaling pathways associated with the CRC carcinogenesis.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>32258125</pmid><doi>10.1155/2020/5201587</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0002-7568-0595</orcidid><orcidid>https://orcid.org/0000-0002-1764-4748</orcidid><oa>free_for_read</oa></addata></record>
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subjects Adenoma
Adult
Aged
Aged, 80 and over
Antigens
Arrays
Bioinformatics
Cancer
Carcinogenesis
Carcinogens
Colorectal cancer
Colorectal carcinoma
Colorectal Neoplasms - metabolism
Colorectal Neoplasms - pathology
Colorectal Neoplasms - virology
Deoxyribonucleic acid
Development and progression
DNA
Ethics
Female
Gene expression
Gene Expression Regulation, Neoplastic
Gene mutations
Genes
Genetic aspects
Genomes
Genomics
Health aspects
Human papillomavirus
Humans
Infections
Male
Matrilysin
Metastasis
Middle Aged
Mutation
Myc protein
Neoplasm Proteins - biosynthesis
Papillomaviridae - metabolism
Papillomavirus infections
Papillomavirus Infections - metabolism
Papillomavirus Infections - pathology
Papillomaviruses
Pathogenesis
Patients
Plates
Proteomics
Sample size
Signal transduction
Signaling
Software
Tissues
Tumors
Wnt protein
title Gene Expression Analysis of Human Papillomavirus-Associated Colorectal Carcinoma
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