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DNA病毒在人类癌症中的作用。

The Role of DNA Viruses in Human Cancer.

作者信息

Ghoreshi Zohreh-Al-Sadat, Molaei Hamid Reza, Arefinia Nasir

机构信息

Student Research Committee, Jiroft University of Medical Sciences, Jiroft, Iran.

Department of Medical Bacteriology and Virology, Faculty of Medicine, Kerman University of Medical Sciences, Kerman, Iran.

出版信息

Cancer Inform. 2023 Jun 13;22:11769351231154186. doi: 10.1177/11769351231154186. eCollection 2023.

DOI:10.1177/11769351231154186
PMID:37363356
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10286548/
Abstract

This review discusses the possible involvement of infections-associated cancers in humans, with virus infections contributing 15% to 20% of total cancer cases in humans. DNA virus encoded proteins interact with host cellular signaling pathways and control proliferation, cell death and genomic integrity viral oncoproteins are known to bind cellular Deubiquitinates (DUBs) such as cyclindromatosis tumor suppressor, ubiquitin-specific proteases 7, 11, 15 and 20, and A-20 to improve their intracellular stability and cellular signaling pathways and finally transformation. Human papillomaviruses (cervical carcinoma, oral cancer and laryngeal cancer); human polyomaviruses (mesotheliomas, brain tumors); Epstein-Barr virus (B-cell lymphoproliferative diseases and nasopharyngeal carcinoma); Kaposi's Sarcoma Herpesvirus (Kaposi's Sarcoma and primary effusion lymphomas); hepatitis B (hepatocellular carcinoma (HCC)) cause up to 20% of malignancies around the world.

摘要

本综述讨论了感染相关癌症在人类中的可能参与情况,病毒感染占人类癌症病例总数的15%至20%。DNA病毒编码的蛋白质与宿主细胞信号通路相互作用,控制细胞增殖、细胞死亡和基因组完整性。已知病毒癌蛋白可结合细胞去泛素化酶(DUBs),如圆柱瘤肿瘤抑制因子、泛素特异性蛋白酶7、11、15和20以及A-20,以提高其细胞内稳定性和细胞信号通路,最终导致细胞转化。人乳头瘤病毒(宫颈癌、口腔癌和喉癌);人多瘤病毒(间皮瘤、脑肿瘤);爱泼斯坦-巴尔病毒(B细胞淋巴增殖性疾病和鼻咽癌);卡波西肉瘤疱疹病毒(卡波西肉瘤和原发性渗出性淋巴瘤);乙型肝炎(肝细胞癌(HCC))导致全球约20%的恶性肿瘤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7456/10286548/bfd50716d312/10.1177_11769351231154186-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7456/10286548/9524b7189487/10.1177_11769351231154186-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7456/10286548/e889408cd662/10.1177_11769351231154186-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7456/10286548/936a77fa87d0/10.1177_11769351231154186-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7456/10286548/14e945538495/10.1177_11769351231154186-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7456/10286548/faa77c16f96f/10.1177_11769351231154186-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7456/10286548/bfd50716d312/10.1177_11769351231154186-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7456/10286548/9524b7189487/10.1177_11769351231154186-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7456/10286548/e889408cd662/10.1177_11769351231154186-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7456/10286548/936a77fa87d0/10.1177_11769351231154186-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7456/10286548/14e945538495/10.1177_11769351231154186-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7456/10286548/faa77c16f96f/10.1177_11769351231154186-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7456/10286548/bfd50716d312/10.1177_11769351231154186-fig6.jpg

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