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HBx Mediated Increase of DDX17 Contributes to HBV-Related Hepatocellular Carcinoma Tumorigenesis
HBV is strongly associated with HCC development and DEAD-box RNA helicase 17 (DDX17) is a very important member of the DEAD box family that plays key roles in HCC development by promoting cancer metastasis. However, the important role of DDX17 in the pathogenesis of HBV-related HCC remains unclear....
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9243429/ https://www.ncbi.nlm.nih.gov/pubmed/35784274 http://dx.doi.org/10.3389/fimmu.2022.871558 |
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author | Dong, Mei-Ling Wen, Xu He, Xin Ren, Ji-Hua Yu, Hai-Bo Qin, Yi-Ping Yang, Zhen Yang, Min-Li Zhou, Chong-Yang Zhang, Hui Cheng, Sheng-Tao Chen, Juan |
author_facet | Dong, Mei-Ling Wen, Xu He, Xin Ren, Ji-Hua Yu, Hai-Bo Qin, Yi-Ping Yang, Zhen Yang, Min-Li Zhou, Chong-Yang Zhang, Hui Cheng, Sheng-Tao Chen, Juan |
author_sort | Dong, Mei-Ling |
collection | PubMed |
description | HBV is strongly associated with HCC development and DEAD-box RNA helicase 17 (DDX17) is a very important member of the DEAD box family that plays key roles in HCC development by promoting cancer metastasis. However, the important role of DDX17 in the pathogenesis of HBV-related HCC remains unclear. In this study, we investigated the role of DDX17 in the replication of HBV and the development of HBV-associated HCC. Based on data from the GEO database and HBV-infected cells, we found that DDX17 was upregulated by the HBV viral protein X (HBx). Mechanistically, increased DDX17 expression promoted HBV replication and transcription by upregulating ZWINT. Further study showed that DDX17 could promote HBx-mediated HCC metastasis. Finally, the promotive effect of DDX17 on HBV and HBV-related HCC was confirmed in vivo. In summary, the results revealed the novel role of DDX17 in the replication of HBV and the metastasis of HBV-associated HCC. |
format | Online Article Text |
id | pubmed-9243429 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-92434292022-07-01 HBx Mediated Increase of DDX17 Contributes to HBV-Related Hepatocellular Carcinoma Tumorigenesis Dong, Mei-Ling Wen, Xu He, Xin Ren, Ji-Hua Yu, Hai-Bo Qin, Yi-Ping Yang, Zhen Yang, Min-Li Zhou, Chong-Yang Zhang, Hui Cheng, Sheng-Tao Chen, Juan Front Immunol Immunology HBV is strongly associated with HCC development and DEAD-box RNA helicase 17 (DDX17) is a very important member of the DEAD box family that plays key roles in HCC development by promoting cancer metastasis. However, the important role of DDX17 in the pathogenesis of HBV-related HCC remains unclear. In this study, we investigated the role of DDX17 in the replication of HBV and the development of HBV-associated HCC. Based on data from the GEO database and HBV-infected cells, we found that DDX17 was upregulated by the HBV viral protein X (HBx). Mechanistically, increased DDX17 expression promoted HBV replication and transcription by upregulating ZWINT. Further study showed that DDX17 could promote HBx-mediated HCC metastasis. Finally, the promotive effect of DDX17 on HBV and HBV-related HCC was confirmed in vivo. In summary, the results revealed the novel role of DDX17 in the replication of HBV and the metastasis of HBV-associated HCC. Frontiers Media S.A. 2022-06-16 /pmc/articles/PMC9243429/ /pubmed/35784274 http://dx.doi.org/10.3389/fimmu.2022.871558 Text en Copyright © 2022 Dong, Wen, He, Ren, Yu, Qin, Yang, Yang, Zhou, Zhang, Cheng and Chen https://creativecommons.org/licenses/by/4.0/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. |
spellingShingle | Immunology Dong, Mei-Ling Wen, Xu He, Xin Ren, Ji-Hua Yu, Hai-Bo Qin, Yi-Ping Yang, Zhen Yang, Min-Li Zhou, Chong-Yang Zhang, Hui Cheng, Sheng-Tao Chen, Juan HBx Mediated Increase of DDX17 Contributes to HBV-Related Hepatocellular Carcinoma Tumorigenesis |
title | HBx Mediated Increase of DDX17 Contributes to HBV-Related Hepatocellular Carcinoma Tumorigenesis |
title_full | HBx Mediated Increase of DDX17 Contributes to HBV-Related Hepatocellular Carcinoma Tumorigenesis |
title_fullStr | HBx Mediated Increase of DDX17 Contributes to HBV-Related Hepatocellular Carcinoma Tumorigenesis |
title_full_unstemmed | HBx Mediated Increase of DDX17 Contributes to HBV-Related Hepatocellular Carcinoma Tumorigenesis |
title_short | HBx Mediated Increase of DDX17 Contributes to HBV-Related Hepatocellular Carcinoma Tumorigenesis |
title_sort | hbx mediated increase of ddx17 contributes to hbv-related hepatocellular carcinoma tumorigenesis |
topic | Immunology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9243429/ https://www.ncbi.nlm.nih.gov/pubmed/35784274 http://dx.doi.org/10.3389/fimmu.2022.871558 |
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