MersV1, Main, Merge, bibRecord, 002394

Hepatitis B virus X protein stabilizes amplified in breast cancer 1 protein and cooperates with it to promote human hepatocellular carcinoma cell invasiveness

Identifieur interne : 002394 ( Main/Merge ); précédent : 002393; suivant : 002395

Hepatitis B virus X protein stabilizes amplified in breast cancer 1 protein and cooperates with it to promote human hepatocellular carcinoma cell invasiveness

Auteurs : Yonghong Liu [République populaire de Chine] ; Zhangwei Tong [République populaire de Chine] ; Ting Li [République populaire de Chine] ; Qiang Chen [République populaire de Chine] ; Luting Zhuo [République populaire de Chine] ; Wengang Li [République populaire de Chine] ; Ray-Chang Wu [États-Unis] ; Chundong Yu [République populaire de Chine]

Source :

Hepatology [ 0270-9139 ] ; 2012-09.

RBID : ISTEX:CA888C09927599F287F6B1ABD9E8D36D37C700F6

English descriptors

Teeft :
- Aib1, Aib1 expression, Aib1 protein, Aib1 protein level, Androgen, Androgen receptor, Assay, Breast cancer, Carcinoma, Cell invasiveness, Cell lines, Cell proliferation, Degradation, Expression plasmids, Fbw7a, Hepatocellular, Hepatology, Hepg2, Hepg2 cells, Important role, Interacted, Invasiveness, Oncogene, Overexpression, Pathway, Plasmid, Promoter, Promoter activity, Protein level, Receptor, Transcription, Transcription factors, Ubiquitination, Xiamen, Xiamen university.

Abstract

Chronic infection of hepatitis B virus (HBV) is closely associated with the development of human hepatocellular carcinoma (HCC). HBV X protein (HBx) plays a key role in the progression of HCC. We recently found that amplified in breast cancer 1 (AIB1) protein is overexpressed in 68% of human HCC specimens and promotes HCC progression by enhancing cell proliferation and invasiveness. Given that both HBx and AIB1 play important oncogenic roles in HCC, we aimed to determine whether they could cooperatively promote human HCC development. Herein, we show that HBx‐positive HCC tissues had a higher level of AIB1 protein, compared to HBx‐negative HCC tissues. A positive correlation between HBx protein level and AIB1 protein level was established in HCC specimens. Without affecting its messenger RNA level, HBx induced a significant increase of the protein level of AIB1, which correlated with a significant extension of the half‐life of AIB1 protein. Mechanistically, HBx could interact with AIB1 to prevent the interaction between envelope protein 3 ubiquitin ligase F‐box and WD repeat domain containing 7 (Fbw7)α and AIB1, then inhibited the Fbw7α‐mediated ubiquitination and degradation of AIB1. In addition, reporter assays and chromatin immunoprecipitation assays revealed that both HBx and AIB1 were recruited to matrix metalloproteinase‐9 (MMP‐9) promoter to enhance MMP‐9 promoter activity cooperatively. Consistently, HBx and AIB1 cooperatively enhanced MMP‐9 expression in HepG2 cells, which, in turn, increased cell‐invasive ability. Conclusion: Our study demonstrates that HBx can stabilize AIB1 protein and cooperate with it to promote human HCC cell invasiveness, highlighting the essential role of the cross‐talk between HBx and AIB1 in HBV‐related HCC progression. (HEPATOLOGY 2012;56:1015–1024)

Url:

https://api.istex.fr/ark:/67375/WNG-6HZ22ZK2-Q/fulltext.pdf

DOI: 10.1002/hep.25751

Links toward previous steps (curation, corpus...)

to stream Istex, to step Corpus: 001471
to stream Istex, to step Curation: 001471
to stream Istex, to step Checkpoint: 000386

Links to Exploration step

ISTEX:CA888C09927599F287F6B1ABD9E8D36D37C700F6

Le document en format XML

<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Hepatitis B virus X protein stabilizes amplified in breast cancer 1 protein and cooperates with it to promote human hepatocellular carcinoma cell invasiveness</title>
<author><name sortKey="Liu, Yonghong" sort="Liu, Yonghong" uniqKey="Liu Y" first="Yonghong" last="Liu">Yonghong Liu</name>
</author>
<author><name sortKey="Tong, Zhangwei" sort="Tong, Zhangwei" uniqKey="Tong Z" first="Zhangwei" last="Tong">Zhangwei Tong</name>
</author>
<author><name sortKey="Li, Ting" sort="Li, Ting" uniqKey="Li T" first="Ting" last="Li">Ting Li</name>
</author>
<author><name sortKey="Chen, Qiang" sort="Chen, Qiang" uniqKey="Chen Q" first="Qiang" last="Chen">Qiang Chen</name>
</author>
<author><name sortKey="Zhuo, Luting" sort="Zhuo, Luting" uniqKey="Zhuo L" first="Luting" last="Zhuo">Luting Zhuo</name>
</author>
<author><name sortKey="Li, Wengang" sort="Li, Wengang" uniqKey="Li W" first="Wengang" last="Li">Wengang Li</name>
</author>
<author><name sortKey="Wu, Ray Hang" sort="Wu, Ray Hang" uniqKey="Wu R" first="Ray-Chang" last="Wu">Ray-Chang Wu</name>
</author>
<author><name sortKey="Yu, Chundong" sort="Yu, Chundong" uniqKey="Yu C" first="Chundong" last="Yu">Chundong Yu</name>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">ISTEX</idno>
<idno type="RBID">ISTEX:CA888C09927599F287F6B1ABD9E8D36D37C700F6</idno>
<date when="2012" year="2012">2012</date>
<idno type="doi">10.1002/hep.25751</idno>
<idno type="url">https://api.istex.fr/ark:/67375/WNG-6HZ22ZK2-Q/fulltext.pdf</idno>
<idno type="wicri:Area/Istex/Corpus">001471</idno>
<idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001471</idno>
<idno type="wicri:Area/Istex/Curation">001471</idno>
<idno type="wicri:Area/Istex/Checkpoint">000386</idno>
<idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Checkpoint">000386</idno>
<idno type="wicri:doubleKey">0270-9139:2012:Liu Y:hepatitis:b:virus</idno>
<idno type="wicri:Area/Main/Merge">002394</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title level="a" type="main">Hepatitis B virus X protein stabilizes amplified in breast cancer 1 protein and cooperates with it to promote human hepatocellular carcinoma cell invasiveness</title>
<author><name sortKey="Liu, Yonghong" sort="Liu, Yonghong" uniqKey="Liu Y" first="Yonghong" last="Liu">Yonghong Liu</name>
<affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen</wicri:regionArea>
<wicri:noRegion>Xiamen</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><country wicri:rule="url">République populaire de Chine</country>
</affiliation>
<affiliation wicri:level="1"><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country>
<wicri:regionArea>Correspondence address: State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen 361005</wicri:regionArea>
<wicri:noRegion>Xiamen 361005</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Tong, Zhangwei" sort="Tong, Zhangwei" uniqKey="Tong Z" first="Zhangwei" last="Tong">Zhangwei Tong</name>
<affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen</wicri:regionArea>
<wicri:noRegion>Xiamen</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Li, Ting" sort="Li, Ting" uniqKey="Li T" first="Ting" last="Li">Ting Li</name>
<affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen</wicri:regionArea>
<wicri:noRegion>Xiamen</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Chen, Qiang" sort="Chen, Qiang" uniqKey="Chen Q" first="Qiang" last="Chen">Qiang Chen</name>
<affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen</wicri:regionArea>
<wicri:noRegion>Xiamen</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>The First Affiliated Hospital of Xiamen University, Xiamen</wicri:regionArea>
<wicri:noRegion>Xiamen</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Zhuo, Luting" sort="Zhuo, Luting" uniqKey="Zhuo L" first="Luting" last="Zhuo">Luting Zhuo</name>
<affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen</wicri:regionArea>
<wicri:noRegion>Xiamen</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Li, Wengang" sort="Li, Wengang" uniqKey="Li W" first="Wengang" last="Li">Wengang Li</name>
<affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Hepatobiliary Pancreas and Vessel Surgery, Chenggong Hospital of Xiamen University, Xiamen</wicri:regionArea>
<wicri:noRegion>Xiamen</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Wu, Ray Hang" sort="Wu, Ray Hang" uniqKey="Wu R" first="Ray-Chang" last="Wu">Ray-Chang Wu</name>
<affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country>
<placeName><region type="state">District de Columbia</region>
</placeName>
<wicri:cityArea>Department of Biochemistry and Molecular Biology, George Washington University Medical Center, Washington</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Yu, Chundong" sort="Yu, Chundong" uniqKey="Yu C" first="Chundong" last="Yu">Chundong Yu</name>
<affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen</wicri:regionArea>
<wicri:noRegion>Xiamen</wicri:noRegion>
</affiliation>
</author>
</analytic>
<monogr></monogr>
<series><title level="j" type="main">Hepatology</title>
<title level="j" type="alt">HEPATOLOGY</title>
<idno type="ISSN">0270-9139</idno>
<idno type="eISSN">1527-3350</idno>
<imprint><biblScope unit="vol">56</biblScope>
<biblScope unit="issue">3</biblScope>
<biblScope unit="page" from="1015">1015</biblScope>
<biblScope unit="page" to="1024">1024</biblScope>
<biblScope unit="page-count">10</biblScope>
<publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher>
<pubPlace>Hoboken</pubPlace>
<date type="published" when="2012-09">2012-09</date>
</imprint>
<idno type="ISSN">0270-9139</idno>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><idno type="ISSN">0270-9139</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Aib1</term>
<term>Aib1 expression</term>
<term>Aib1 protein</term>
<term>Aib1 protein level</term>
<term>Androgen</term>
<term>Androgen receptor</term>
<term>Assay</term>
<term>Breast cancer</term>
<term>Carcinoma</term>
<term>Cell invasiveness</term>
<term>Cell lines</term>
<term>Cell proliferation</term>
<term>Degradation</term>
<term>Expression plasmids</term>
<term>Fbw7a</term>
<term>Hepatocellular</term>
<term>Hepatology</term>
<term>Hepg2</term>
<term>Hepg2 cells</term>
<term>Important role</term>
<term>Interacted</term>
<term>Invasiveness</term>
<term>Oncogene</term>
<term>Overexpression</term>
<term>Pathway</term>
<term>Plasmid</term>
<term>Promoter</term>
<term>Promoter activity</term>
<term>Protein level</term>
<term>Receptor</term>
<term>Transcription</term>
<term>Transcription factors</term>
<term>Ubiquitination</term>
<term>Xiamen</term>
<term>Xiamen university</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Chronic infection of hepatitis B virus (HBV) is closely associated with the development of human hepatocellular carcinoma (HCC). HBV X protein (HBx) plays a key role in the progression of HCC. We recently found that amplified in breast cancer 1 (AIB1) protein is overexpressed in 68% of human HCC specimens and promotes HCC progression by enhancing cell proliferation and invasiveness. Given that both HBx and AIB1 play important oncogenic roles in HCC, we aimed to determine whether they could cooperatively promote human HCC development. Herein, we show that HBx‐positive HCC tissues had a higher level of AIB1 protein, compared to HBx‐negative HCC tissues. A positive correlation between HBx protein level and AIB1 protein level was established in HCC specimens. Without affecting its messenger RNA level, HBx induced a significant increase of the protein level of AIB1, which correlated with a significant extension of the half‐life of AIB1 protein. Mechanistically, HBx could interact with AIB1 to prevent the interaction between envelope protein 3 ubiquitin ligase F‐box and WD repeat domain containing 7 (Fbw7)α and AIB1, then inhibited the Fbw7α‐mediated ubiquitination and degradation of AIB1. In addition, reporter assays and chromatin immunoprecipitation assays revealed that both HBx and AIB1 were recruited to matrix metalloproteinase‐9 (MMP‐9) promoter to enhance MMP‐9 promoter activity cooperatively. Consistently, HBx and AIB1 cooperatively enhanced MMP‐9 expression in HepG2 cells, which, in turn, increased cell‐invasive ability. Conclusion: Our study demonstrates that HBx can stabilize AIB1 protein and cooperate with it to promote human HCC cell invasiveness, highlighting the essential role of the cross‐talk between HBx and AIB1 in HBV‐related HCC progression. (HEPATOLOGY 2012;56:1015–1024)</div>
</front>
</TEI>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Sante/explor/MersV1/Data/Main/Merge

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 002394 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/Main/Merge/biblio.hfd -nk 002394 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Sante
   |area=    MersV1
   |flux=    Main
   |étape=   Merge
   |type=    RBID
   |clé=     ISTEX:CA888C09927599F287F6B1ABD9E8D36D37C700F6
   |texte=   Hepatitis B virus X protein stabilizes amplified in breast cancer 1 protein and cooperates with it to promote human hepatocellular carcinoma cell invasiveness
}}

This area was generated with Dilib version V0.6.33.
Data generation: Mon Apr 20 23:26:43 2020. Site generation: Sat Mar 27 09:06:09 2021

	Serveur d'exploration MERS
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration MERS

Hepatitis B virus X protein stabilizes amplified in breast cancer 1 protein and cooperates with it to promote human hepatocellular carcinoma cell invasiveness

Hepatitis B virus X protein stabilizes amplified in breast cancer 1 protein and cooperates with it to promote human hepatocellular carcinoma cell invasiveness

Source :

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri