{"title":"基于毒物基因组学鉴定全氟化合物诱发人类癌症的潜在机制和信号通路。","authors":"Zahra Dehghani, Sara Ranjbar, Farbod Shahabinezhad, Pooria Sabouri, Afshin Mohammadi Bardbori","doi":"10.1093/toxres/tfae151","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>The number of new diagnosed cancer cases and cancer deaths are increasing worldwide. Perfluorinated compounds (PFCs) are synthetic chemicals, which are possible inducers of cancer in human and laboratory animals. Studies showed that PFCs induce breast, prostate, kidney, liver and pancreas cancer by inducing genes being involved in carcinogenic pathways.</p><p><strong>Methodology: </strong>This study reviews the association between PFCs induced up-regulation/down-regulation of genes and signaling pathways that are important in promoting different types of cancer. To obtain chemical-gene interactions, an advanced search was performed in the Comparative Toxicogenomics Database platform.</p><p><strong>Results: </strong>Five most prevalent cancers were studied and the maps of their signaling pathways were drawn, and colored borders indicate significantly differentially expressed genes if there had been reports of alterations in expression in the presence of PFCs.</p><p><strong>Conclusion: </strong>In general, PFCs are capable of inducing cancer in human via altering PPARα and PI3K pathways, evading apoptosis, inducing sustained angiogenesis, alterations in proliferation and blocking differentiation. However, more epidemiological data and mechanistic studies are needed to better understand the carcinogenic effects of PFCs in human.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 5","pages":"tfae151"},"PeriodicalIF":2.2000,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11420517/pdf/","citationCount":"0","resultStr":"{\"title\":\"A toxicogenomics-based identification of potential mechanisms and signaling pathways involved in PFCs-induced cancer in human.\",\"authors\":\"Zahra Dehghani, Sara Ranjbar, Farbod Shahabinezhad, Pooria Sabouri, Afshin Mohammadi Bardbori\",\"doi\":\"10.1093/toxres/tfae151\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>The number of new diagnosed cancer cases and cancer deaths are increasing worldwide. Perfluorinated compounds (PFCs) are synthetic chemicals, which are possible inducers of cancer in human and laboratory animals. Studies showed that PFCs induce breast, prostate, kidney, liver and pancreas cancer by inducing genes being involved in carcinogenic pathways.</p><p><strong>Methodology: </strong>This study reviews the association between PFCs induced up-regulation/down-regulation of genes and signaling pathways that are important in promoting different types of cancer. To obtain chemical-gene interactions, an advanced search was performed in the Comparative Toxicogenomics Database platform.</p><p><strong>Results: </strong>Five most prevalent cancers were studied and the maps of their signaling pathways were drawn, and colored borders indicate significantly differentially expressed genes if there had been reports of alterations in expression in the presence of PFCs.</p><p><strong>Conclusion: </strong>In general, PFCs are capable of inducing cancer in human via altering PPARα and PI3K pathways, evading apoptosis, inducing sustained angiogenesis, alterations in proliferation and blocking differentiation. However, more epidemiological data and mechanistic studies are needed to better understand the carcinogenic effects of PFCs in human.</p>\",\"PeriodicalId\":105,\"journal\":{\"name\":\"Toxicology Research\",\"volume\":\"13 5\",\"pages\":\"tfae151\"},\"PeriodicalIF\":2.2000,\"publicationDate\":\"2024-09-24\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11420517/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Toxicology Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1093/toxres/tfae151\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/10/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q3\",\"JCRName\":\"TOXICOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Toxicology Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1093/toxres/tfae151","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/10/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"TOXICOLOGY","Score":null,"Total":0}
A toxicogenomics-based identification of potential mechanisms and signaling pathways involved in PFCs-induced cancer in human.
Introduction: The number of new diagnosed cancer cases and cancer deaths are increasing worldwide. Perfluorinated compounds (PFCs) are synthetic chemicals, which are possible inducers of cancer in human and laboratory animals. Studies showed that PFCs induce breast, prostate, kidney, liver and pancreas cancer by inducing genes being involved in carcinogenic pathways.
Methodology: This study reviews the association between PFCs induced up-regulation/down-regulation of genes and signaling pathways that are important in promoting different types of cancer. To obtain chemical-gene interactions, an advanced search was performed in the Comparative Toxicogenomics Database platform.
Results: Five most prevalent cancers were studied and the maps of their signaling pathways were drawn, and colored borders indicate significantly differentially expressed genes if there had been reports of alterations in expression in the presence of PFCs.
Conclusion: In general, PFCs are capable of inducing cancer in human via altering PPARα and PI3K pathways, evading apoptosis, inducing sustained angiogenesis, alterations in proliferation and blocking differentiation. However, more epidemiological data and mechanistic studies are needed to better understand the carcinogenic effects of PFCs in human.