The Tumor Suppressor, p53, Negatively Regulates Non-Canonical NF-κB Signaling through miRNA-Induced Silencing of NF-κB–Inducing Kinase
Identifieur interne : 000353 ( Main/Curation ); précédent : 000352; suivant : 000354The Tumor Suppressor, p53, Negatively Regulates Non-Canonical NF-κB Signaling through miRNA-Induced Silencing of NF-κB–Inducing Kinase
Auteurs : Hanbit Jang [Corée du Sud] ; Seulki Park [Corée du Sud] ; Jaehoon Kim [Corée du Sud] ; Jong Hwan Kim [Corée du Sud] ; Seon-Young Kim [Corée du Sud] ; Sayeon Cho [Corée du Sud] ; Sung Goo Park [Corée du Sud] ; Byoung Chul Park [Corée du Sud] ; Sunhong Kim [Corée du Sud] ; Jeong-Hoon Kim [Corée du Sud]Source :
- Molecules and Cells [ 1016-8478 ] ; 2019.
Abstract
NF-κB signaling through both canonical and non-canonical pathways plays a central role in immune responses and inflammation. NF-κB–inducing kinase (NIK) stabilization is a key step in activation of the non-canonical pathway and its dysregulation implicated in various hematologic malignancies. The tumor suppressor, p53, is an established cellular gatekeeper of proliferation. Abnormalities of the
Url:
DOI: 10.14348/molcells.2019.0239
PubMed: 31870133
PubMed Central: 6999715
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PMC:6999715Le document en format XML
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<country xml:lang="fr">Corée du Sud</country>
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<affiliation wicri:level="1"><nlm:aff id="af2-molce-43-023">Disease Target Structure Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 34141,<country>Korea</country>
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<author><name sortKey="Park, Seulki" sort="Park, Seulki" uniqKey="Park S" first="Seulki" last="Park">Seulki Park</name>
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<affiliation wicri:level="1"><nlm:aff id="af3-molce-43-023">Department of Functional Genomics, KRIBB School of Bioscience, Korea University of Science and Technology, Daejeon 34113,<country>Korea</country>
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<author><name sortKey="Kim, Jaehoon" sort="Kim, Jaehoon" uniqKey="Kim J" first="Jaehoon" last="Kim">Jaehoon Kim</name>
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<author><name sortKey="Kim, Jong Hwan" sort="Kim, Jong Hwan" uniqKey="Kim J" first="Jong Hwan" last="Kim">Jong Hwan Kim</name>
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<author><name sortKey="Kim, Seon Young" sort="Kim, Seon Young" uniqKey="Kim S" first="Seon-Young" last="Kim">Seon-Young Kim</name>
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<author><name sortKey="Cho, Sayeon" sort="Cho, Sayeon" uniqKey="Cho S" first="Sayeon" last="Cho">Sayeon Cho</name>
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</nlm:aff>
<country xml:lang="fr">Corée du Sud</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Park, Sung Goo" sort="Park, Sung Goo" uniqKey="Park S" first="Sung Goo" last="Park">Sung Goo Park</name>
<affiliation wicri:level="1"><nlm:aff id="af2-molce-43-023">Disease Target Structure Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 34141,<country>Korea</country>
</nlm:aff>
<country xml:lang="fr">Corée du Sud</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
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<affiliation wicri:level="1"><nlm:aff id="af3-molce-43-023">Department of Functional Genomics, KRIBB School of Bioscience, Korea University of Science and Technology, Daejeon 34113,<country>Korea</country>
</nlm:aff>
<country xml:lang="fr">Corée du Sud</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
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<author><name sortKey="Park, Byoung Chul" sort="Park, Byoung Chul" uniqKey="Park B" first="Byoung Chul" last="Park">Byoung Chul Park</name>
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</nlm:aff>
<country xml:lang="fr">Corée du Sud</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="af4-molce-43-023">Department of Proteome Structural Biology, KRIBB School of Bioscience, Korea University of Science and Technology, Daejeon 34113,<country>Korea</country>
</nlm:aff>
<country xml:lang="fr">Corée du Sud</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
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<author><name sortKey="Kim, Sunhong" sort="Kim, Sunhong" uniqKey="Kim S" first="Sunhong" last="Kim">Sunhong Kim</name>
<affiliation wicri:level="1"><nlm:aff id="af2-molce-43-023">Disease Target Structure Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 34141,<country>Korea</country>
</nlm:aff>
<country xml:lang="fr">Corée du Sud</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="af5-molce-43-023">Department of Bio-Molecular Science, KRIBB School of Bioscience, Korea University of Science and Technology, Daejeon 34113,<country>Korea</country>
</nlm:aff>
<country xml:lang="fr">Corée du Sud</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Kim, Jeong Hoon" sort="Kim, Jeong Hoon" uniqKey="Kim J" first="Jeong-Hoon" last="Kim">Jeong-Hoon Kim</name>
<affiliation wicri:level="1"><nlm:aff id="af2-molce-43-023">Disease Target Structure Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 34141,<country>Korea</country>
</nlm:aff>
<country xml:lang="fr">Corée du Sud</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="af3-molce-43-023">Department of Functional Genomics, KRIBB School of Bioscience, Korea University of Science and Technology, Daejeon 34113,<country>Korea</country>
</nlm:aff>
<country xml:lang="fr">Corée du Sud</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
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<series><title level="j">Molecules and Cells</title>
<idno type="ISSN">1016-8478</idno>
<idno type="eISSN">0219-1032</idno>
<imprint><date when="2019">2019</date>
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<front><div type="abstract" xml:lang="en"><p>NF-κB signaling through both canonical and non-canonical pathways plays a central role in immune responses and inflammation. NF-κB–inducing kinase (NIK) stabilization is a key step in activation of the non-canonical pathway and its dysregulation implicated in various hematologic malignancies. The tumor suppressor, p53, is an established cellular gatekeeper of proliferation. Abnormalities of the <italic>TP53</italic>
gene have been detected in more than half of all human cancers. While the non-canonical NF-κB and p53 pathways have been explored for several decades, no studies to date have documented potential cross-talk between these two cancer-related mechanisms. Here, we demonstrate that p53 negatively regulates NIK in an miRNA-dependent manner. Overexpression of p53 decreased the levels of NIK, leading to inhibition of the non-canonical NF-κB pathway. Conversely, its knockdown led to increased levels of NIK, IKKα phosphorylation, and p100 processing. Additionally, miR-34b induced by nutlin-3 directly targeted the coding sequences (CDS) of NIK. Treatment with anti-miR-34b-5p augmented NIK levels and subsequent non-canonical NF-κB signaling. Our collective findings support a novel cross-talk mechanism between non-canonical NF-κB and p53.</p>
</div>
</front>
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