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HBx and c-MYC Cooperate to Induce URI1 Expression in HBV-Related Hepatocellular Carcinoma

Unconventional prefoldin RNA polymerase II subunit 5 interactor (URI1) has emerged as an oncogenic driver in hepatocellular carcinoma (HCC). Although the hepatitis B virus (HBV) represents the most common etiology of HCC worldwide, it is unknown whether URI1 plays a role in HBV-related HCC (HCC-B)....

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Detalles Bibliográficos
Autores principales: Tsuchiya, Hiroyuki, Amisaki, Masataka, Takenaga, Ai, Honjo, Soichiro, Fujiwara, Yoshiyuki, Shiota, Goshi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6888623/
https://www.ncbi.nlm.nih.gov/pubmed/31739577
http://dx.doi.org/10.3390/ijms20225714
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author Tsuchiya, Hiroyuki
Amisaki, Masataka
Takenaga, Ai
Honjo, Soichiro
Fujiwara, Yoshiyuki
Shiota, Goshi
author_facet Tsuchiya, Hiroyuki
Amisaki, Masataka
Takenaga, Ai
Honjo, Soichiro
Fujiwara, Yoshiyuki
Shiota, Goshi
author_sort Tsuchiya, Hiroyuki
collection PubMed
description Unconventional prefoldin RNA polymerase II subunit 5 interactor (URI1) has emerged as an oncogenic driver in hepatocellular carcinoma (HCC). Although the hepatitis B virus (HBV) represents the most common etiology of HCC worldwide, it is unknown whether URI1 plays a role in HBV-related HCC (HCC-B). In the present study, we investigated URI1 expression and its underlying mechanism in HCC-B tissues and cell lines. URI1 gene-promoter activity was determined by a luciferase assay. Human HCC-B samples were used for a chromatin immunoprecipitation assay. We found that c-MYC induced URI1 expression and activated the URI1 promoter through the E-box in the promoter region while the HBx protein significantly enhanced it. The positivity of URI1 expression was significantly higher in HCC-B tumor tissues than in non-HBV-related HCC tumor tissues, suggesting that a specific mechanism underlies URI1 expression in HCC-B. In tumor tissues from HCC-B patients, a significantly higher level of c-MYC was recruited to the E-box than in non-tumor tissues. These results suggest that HBx and c-MYC are involved in URI1 expression in HCC-B. URI1 expression may play important roles in the development and progression of HCC-B because HBx and c-MYC are well-known oncogenic factors in the virus and host, respectively.
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spelling pubmed-68886232019-12-09 HBx and c-MYC Cooperate to Induce URI1 Expression in HBV-Related Hepatocellular Carcinoma Tsuchiya, Hiroyuki Amisaki, Masataka Takenaga, Ai Honjo, Soichiro Fujiwara, Yoshiyuki Shiota, Goshi Int J Mol Sci Communication Unconventional prefoldin RNA polymerase II subunit 5 interactor (URI1) has emerged as an oncogenic driver in hepatocellular carcinoma (HCC). Although the hepatitis B virus (HBV) represents the most common etiology of HCC worldwide, it is unknown whether URI1 plays a role in HBV-related HCC (HCC-B). In the present study, we investigated URI1 expression and its underlying mechanism in HCC-B tissues and cell lines. URI1 gene-promoter activity was determined by a luciferase assay. Human HCC-B samples were used for a chromatin immunoprecipitation assay. We found that c-MYC induced URI1 expression and activated the URI1 promoter through the E-box in the promoter region while the HBx protein significantly enhanced it. The positivity of URI1 expression was significantly higher in HCC-B tumor tissues than in non-HBV-related HCC tumor tissues, suggesting that a specific mechanism underlies URI1 expression in HCC-B. In tumor tissues from HCC-B patients, a significantly higher level of c-MYC was recruited to the E-box than in non-tumor tissues. These results suggest that HBx and c-MYC are involved in URI1 expression in HCC-B. URI1 expression may play important roles in the development and progression of HCC-B because HBx and c-MYC are well-known oncogenic factors in the virus and host, respectively. MDPI 2019-11-14 /pmc/articles/PMC6888623/ /pubmed/31739577 http://dx.doi.org/10.3390/ijms20225714 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Communication
Tsuchiya, Hiroyuki
Amisaki, Masataka
Takenaga, Ai
Honjo, Soichiro
Fujiwara, Yoshiyuki
Shiota, Goshi
HBx and c-MYC Cooperate to Induce URI1 Expression in HBV-Related Hepatocellular Carcinoma
title HBx and c-MYC Cooperate to Induce URI1 Expression in HBV-Related Hepatocellular Carcinoma
title_full HBx and c-MYC Cooperate to Induce URI1 Expression in HBV-Related Hepatocellular Carcinoma
title_fullStr HBx and c-MYC Cooperate to Induce URI1 Expression in HBV-Related Hepatocellular Carcinoma
title_full_unstemmed HBx and c-MYC Cooperate to Induce URI1 Expression in HBV-Related Hepatocellular Carcinoma
title_short HBx and c-MYC Cooperate to Induce URI1 Expression in HBV-Related Hepatocellular Carcinoma
title_sort hbx and c-myc cooperate to induce uri1 expression in hbv-related hepatocellular carcinoma
topic Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6888623/
https://www.ncbi.nlm.nih.gov/pubmed/31739577
http://dx.doi.org/10.3390/ijms20225714
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