TNFAIP8 regulates autophagy, cell steatosis, and promotes hepatocellular carcinoma cell proliferation
Identifieur interne : 000038 ( an2020/Analysis ); précédent : 000037; suivant : 000039TNFAIP8 regulates autophagy, cell steatosis, and promotes hepatocellular carcinoma cell proliferation
Auteurs : Suryakant Niture [États-Unis] ; Maxwell A. Gyamfi [États-Unis] ; Minghui Lin [États-Unis, République populaire de Chine] ; Uchechukwu Chimeh [États-Unis] ; Xialan Dong [États-Unis] ; Weifan Zheng [États-Unis] ; John Moore [États-Unis] ; Deepak Kumar [États-Unis]Source :
- Cell Death & Disease [ 2041-4889 ] ; 2020.
Abstract
Tumor necrosis factor-α-induced protein 8 (TNFAIP8) expression has been linked to tumor progression in various cancer types, but the detailed mechanisms of TNFAIP8 are not fully elucidated. Here we define the role of TNFAIP8 in early events associated with development of hepatocellular carcinoma (HCC). Increased TNFAIP8 levels in HCC cells enhanced cell survival by blocking apoptosis, rendering HCC cells more resistant to the anticancer drugs, sorafenib and regorafenib. TNFAIP8 also induced autophagy and steatosis in liver cancer cells. Consistent with these observations, TNFAIP8 blocked AKT/mTOR signaling and showed direct interaction with ATG3-ATG7 proteins. TNFAIP8 also exhibited binding with fatty acids and modulated expression of lipid/fatty-acid metabolizing enzymes. Chronic feeding of mice with alcohol increased hepatic levels of TNFAIP8, autophagy, and steatosis but not in high-fat-fed obese mice. Similarly, higher TNFAIP8 expression was associated with steatotic livers of human patients with a history of alcohol use but not in steatotic patients with no history of alcohol use. Our data indicate a novel role of TNFAIP8 in modulation of drug resistance, autophagy, and hepatic steatosis, all key early events in HCC progression.
Url:
DOI: 10.1038/s41419-020-2369-4
PubMed: 32152268
PubMed Central: 7062894
Affiliations:
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Chambers Biomedical Biotechnology Research Institute,</institution><institution>North Carolina Central University Durham,</institution></institution-wrap>Durham, NC 27707 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Caroline du Nord</region></placeName><wicri:cityArea>Durham</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:aff id="Aff4"><institution-wrap><institution-id institution-id-type="ISNI">0000000122955703</institution-id><institution-id institution-id-type="GRID">grid.261038.e</institution-id><institution>Department of Pharmaceutical Sciences,</institution><institution>North Carolina Central University Durham,</institution></institution-wrap>Durham, NC 27707 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Caroline du Nord</region></placeName><wicri:cityArea>Durham</wicri:cityArea></affiliation></author></analytic><series><title level="j">Cell Death & Disease</title><idno type="eISSN">2041-4889</idno><imprint><date when="2020">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="Par1">Tumor necrosis factor-α-induced protein 8 (TNFAIP8) expression has been linked to tumor progression in various cancer types, but the detailed mechanisms of TNFAIP8 are not fully elucidated. Here we define the role of TNFAIP8 in early events associated with development of hepatocellular carcinoma (HCC). Increased TNFAIP8 levels in HCC cells enhanced cell survival by blocking apoptosis, rendering HCC cells more resistant to the anticancer drugs, sorafenib and regorafenib. TNFAIP8 also induced autophagy and steatosis in liver cancer cells. Consistent with these observations, TNFAIP8 blocked AKT/mTOR signaling and showed direct interaction with ATG3-ATG7 proteins. TNFAIP8 also exhibited binding with fatty acids and modulated expression of lipid/fatty-acid metabolizing enzymes. Chronic feeding of mice with alcohol increased hepatic levels of TNFAIP8, autophagy, and steatosis but not in high-fat-fed obese mice. Similarly, higher TNFAIP8 expression was associated with steatotic livers of human patients with a history of alcohol use but not in steatotic patients with no history of alcohol use. Our data indicate a novel role of TNFAIP8 in modulation of drug resistance, autophagy, and hepatic steatosis, all key early events in HCC progression.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Freundt, Ec" uniqKey="Freundt E">EC Freundt</name></author><author><name sortKey="Bidere, N" uniqKey="Bidere N">N Bidere</name></author><author><name sortKey="Lenardo, Mj" uniqKey="Lenardo M">MJ Lenardo</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kumar, D" uniqKey="Kumar D">D Kumar</name></author><author><name sortKey="Whiteside, Tl" uniqKey="Whiteside T">TL Whiteside</name></author><author><name sortKey="Kasid, U" uniqKey="Kasid U">U Kasid</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sun, H" uniqKey="Sun H">H Sun</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Niture, S" uniqKey="Niture S">S 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sortKey="Ding, Wx" uniqKey="Ding W">WX Ding</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Dong, H" uniqKey="Dong H">H Dong</name></author><author><name sortKey="Czaja, Mj" uniqKey="Czaja M">MJ Czaja</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Toshikuni, N" uniqKey="Toshikuni N">N Toshikuni</name></author><author><name sortKey="Tsutsumi, M" uniqKey="Tsutsumi M">M Tsutsumi</name></author><author><name sortKey="Arisawa, T" uniqKey="Arisawa T">T Arisawa</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Mahli, A" uniqKey="Mahli A">A Mahli</name></author><author><name sortKey="Hellerbrand, C" uniqKey="Hellerbrand C">C Hellerbrand</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Boyle, M" uniqKey="Boyle M">M Boyle</name></author><author><name sortKey="Masson, S" uniqKey="Masson S">S Masson</name></author><author><name sortKey="Anstee, Qm" uniqKey="Anstee Q">QM Anstee</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Chao, X" uniqKey="Chao X">X Chao</name></author><author><name sortKey="Ding, Wx" uniqKey="Ding W">WX Ding</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>République populaire de Chine</li><li>États-Unis</li></country><region><li>Caroline du Nord</li></region></list><tree><country name="États-Unis"><region name="Caroline du Nord"><name sortKey="Niture, Suryakant" sort="Niture, Suryakant" uniqKey="Niture S" first="Suryakant" last="Niture">Suryakant Niture</name></region><name sortKey="Chimeh, Uchechukwu" sort="Chimeh, Uchechukwu" uniqKey="Chimeh U" first="Uchechukwu" last="Chimeh">Uchechukwu Chimeh</name><name sortKey="Dong, Xialan" sort="Dong, Xialan" uniqKey="Dong X" first="Xialan" last="Dong">Xialan Dong</name><name sortKey="Gyamfi, Maxwell A" sort="Gyamfi, Maxwell A" uniqKey="Gyamfi M" first="Maxwell A." last="Gyamfi">Maxwell A. Gyamfi</name><name sortKey="Kumar, Deepak" sort="Kumar, Deepak" uniqKey="Kumar D" first="Deepak" last="Kumar">Deepak Kumar</name><name sortKey="Kumar, Deepak" sort="Kumar, Deepak" uniqKey="Kumar D" first="Deepak" last="Kumar">Deepak Kumar</name><name sortKey="Lin, Minghui" sort="Lin, Minghui" uniqKey="Lin M" first="Minghui" last="Lin">Minghui Lin</name><name sortKey="Moore, John" sort="Moore, John" uniqKey="Moore J" first="John" last="Moore">John Moore</name><name sortKey="Zheng, Weifan" sort="Zheng, Weifan" uniqKey="Zheng W" first="Weifan" last="Zheng">Weifan Zheng</name></country><country name="République populaire de Chine"><noRegion><name sortKey="Lin, Minghui" sort="Lin, Minghui" uniqKey="Lin M" first="Minghui" last="Lin">Minghui Lin</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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