Regulation of HPV16 E6 and MCL1 by SF3B1 inhibitor in head and neck cancer cells
Identifieur interne : 001694 ( Main/Exploration ); précédent : 001693; suivant : 001695Regulation of HPV16 E6 and MCL1 by SF3B1 inhibitor in head and neck cancer cells
Auteurs : Yang Gao [États-Unis] ; Sumita Trivedi [États-Unis] ; Robert L. Ferris [États-Unis] ; Kazunori Koide [États-Unis]Source :
- Scientific Reports [ 2045-2322 ] ; 2014.
Descripteurs français
- KwdFr :
- Apoptose (), Caspase-3 (métabolisme), Caspase-7 (métabolisme), Cellules HeLa, Dérivés du biphényle (toxicité), Facteurs d'épissage des ARN, Humains, Interférence par ARN, Lignée cellulaire tumorale, Morpholines (toxicité), Nitrophénols (toxicité), Papillomavirus humain de type 16 (métabolisme), Petit ARN interférent (métabolisme), Petites ribonucléoprotéines nucléaires U2 (antagonistes et inhibiteurs), Petites ribonucléoprotéines nucléaires U2 (génétique), Petites ribonucléoprotéines nucléaires U2 (métabolisme), Phosphoprotéines (antagonistes et inhibiteurs), Phosphoprotéines (génétique), Phosphoprotéines (métabolisme), Pipérazines (toxicité), Protéine Bak (métabolisme), Protéine Bax (métabolisme), Protéine Mcl-1 (génétique), Protéine Mcl-1 (métabolisme), Protéine bcl-X (métabolisme), Protéines de répression (génétique), Protéines de répression (métabolisme), Protéines des oncogènes viraux (génétique), Protéines des oncogènes viraux (métabolisme), Pyrannes (toxicité), Sulfonamides (toxicité), Synergie des médicaments, Tumeurs de la tête et du cou (anatomopathologie), Tumeurs de la tête et du cou (métabolisme), Tumeurs de la tête et du cou (virologie), Épissage des ARN ().
- MESH :
- anatomopathologie : Tumeurs de la tête et du cou.
- antagonistes et inhibiteurs : Petites ribonucléoprotéines nucléaires U2, Phosphoprotéines.
- génétique : Petites ribonucléoprotéines nucléaires U2, Phosphoprotéines, Protéine Mcl-1, Protéines de répression, Protéines des oncogènes viraux.
- métabolisme : Caspase-3, Caspase-7, Papillomavirus humain de type 16, Petit ARN interférent, Petites ribonucléoprotéines nucléaires U2, Phosphoprotéines, Protéine Bak, Protéine Bax, Protéine Mcl-1, Protéine bcl-X, Protéines de répression, Protéines des oncogènes viraux, Tumeurs de la tête et du cou.
- toxicité : Dérivés du biphényle, Morpholines, Nitrophénols, Pipérazines, Pyrannes, Sulfonamides.
- virologie : Tumeurs de la tête et du cou.
- Apoptose, Cellules HeLa, Facteurs d'épissage des ARN, Humains, Interférence par ARN, Lignée cellulaire tumorale, Synergie des médicaments, Épissage des ARN.
English descriptors
- KwdEn :
- Apoptosis (drug effects), Biphenyl Compounds (toxicity), Caspase 3 (metabolism), Caspase 7 (metabolism), Cell Line, Tumor, Drug Synergism, HeLa Cells, Head and Neck Neoplasms (metabolism), Head and Neck Neoplasms (pathology), Head and Neck Neoplasms (virology), Human papillomavirus 16 (metabolism), Humans, Morpholines (toxicity), Myeloid Cell Leukemia Sequence 1 Protein (genetics), Myeloid Cell Leukemia Sequence 1 Protein (metabolism), Nitrophenols (toxicity), Oncogene Proteins, Viral (genetics), Oncogene Proteins, Viral (metabolism), Phosphoproteins (antagonists & inhibitors), Phosphoproteins (genetics), Phosphoproteins (metabolism), Piperazines (toxicity), Pyrans (toxicity), RNA Interference, RNA Splicing (drug effects), RNA Splicing Factors, RNA, Small Interfering (metabolism), Repressor Proteins (genetics), Repressor Proteins (metabolism), Ribonucleoprotein, U2 Small Nuclear (antagonists & inhibitors), Ribonucleoprotein, U2 Small Nuclear (genetics), Ribonucleoprotein, U2 Small Nuclear (metabolism), Sulfonamides (toxicity), bcl-2 Homologous Antagonist-Killer Protein (metabolism), bcl-2-Associated X Protein (metabolism), bcl-X Protein (metabolism).
- MESH :
- chemical , antagonists & inhibitors : Phosphoproteins, Ribonucleoprotein, U2 Small Nuclear.
- chemical , genetics : Myeloid Cell Leukemia Sequence 1 Protein, Oncogene Proteins, Viral, Phosphoproteins, Repressor Proteins, Ribonucleoprotein, U2 Small Nuclear.
- chemical , metabolism : Caspase 3, Caspase 7, Myeloid Cell Leukemia Sequence 1 Protein, Oncogene Proteins, Viral, Phosphoproteins, RNA, Small Interfering, Repressor Proteins, Ribonucleoprotein, U2 Small Nuclear, bcl-2 Homologous Antagonist-Killer Protein, bcl-2-Associated X Protein, bcl-X Protein.
- chemical , toxicity : Biphenyl Compounds, Morpholines, Nitrophenols, Piperazines, Pyrans, Sulfonamides.
- drug effects : Apoptosis, RNA Splicing.
- metabolism : Head and Neck Neoplasms, Human papillomavirus 16.
- pathology : Head and Neck Neoplasms.
- virology : Head and Neck Neoplasms.
- Cell Line, Tumor, Drug Synergism, HeLa Cells, Humans, RNA Interference, RNA Splicing Factors.
Abstract
ABT-737 inhibits the anti-apoptotic proteins B-cell lymphoma 2 (BCL-2) and BCL-XL. Meayamycin B switches the splicing pattern of myeloid cell leukemia factor 1 (MCL1) pre-mRNA. Specifically, inhibition of splicing factor 3B subunit 1 (SF3B1) with meayamycin B promotes the generation of the proapoptotic, short splicing variant (MCL1-S) and diminishes the antiapoptotic, long variant (MCL1-L). This action was previously associated with the cytotoxicity of meayamycin B in non-small cell lung carcinoma cell lines. ABT-737 induced apoptosis in response to an ablation of MCL1-L by meayamycin B. In this study, we further exploited this synergistic combination in head and neck squamous cell carcinoma (HNSCC), up to 90% of which overexpress MCL1 and BCL-XL. In a panel of seven HNSCC cell lines, the combination of meayamycin B and ABT-737 rapidly triggered a Bax/Bak-mediated apoptosis that overcame the resistance from HPV16-positive HNSCC against each agent alone. Both RT-PCR and Western blotting showed that meayamycin B up-regulated MCL1-S and down-regulated MCL1-L. Significantly, we discovered that SF3B1 was involved in the splicing of oncogenic HPV16 E6 to produce non-oncogenic HPV16 E6*, indicating that SF3B1 may inhibit HPV16-induced tumorigenesis.
Url:
DOI: 10.1038/srep06098
PubMed: 25139387
PubMed Central: 4138523
Affiliations:
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Le document en format XML
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<author><name sortKey="Trivedi, Sumita" sort="Trivedi, Sumita" uniqKey="Trivedi S" first="Sumita" last="Trivedi">Sumita Trivedi</name>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis (drug effects)</term>
<term>Biphenyl Compounds (toxicity)</term>
<term>Caspase 3 (metabolism)</term>
<term>Caspase 7 (metabolism)</term>
<term>Cell Line, Tumor</term>
<term>Drug Synergism</term>
<term>HeLa Cells</term>
<term>Head and Neck Neoplasms (metabolism)</term>
<term>Head and Neck Neoplasms (pathology)</term>
<term>Head and Neck Neoplasms (virology)</term>
<term>Human papillomavirus 16 (metabolism)</term>
<term>Humans</term>
<term>Morpholines (toxicity)</term>
<term>Myeloid Cell Leukemia Sequence 1 Protein (genetics)</term>
<term>Myeloid Cell Leukemia Sequence 1 Protein (metabolism)</term>
<term>Nitrophenols (toxicity)</term>
<term>Oncogene Proteins, Viral (genetics)</term>
<term>Oncogene Proteins, Viral (metabolism)</term>
<term>Phosphoproteins (antagonists & inhibitors)</term>
<term>Phosphoproteins (genetics)</term>
<term>Phosphoproteins (metabolism)</term>
<term>Piperazines (toxicity)</term>
<term>Pyrans (toxicity)</term>
<term>RNA Interference</term>
<term>RNA Splicing (drug effects)</term>
<term>RNA Splicing Factors</term>
<term>RNA, Small Interfering (metabolism)</term>
<term>Repressor Proteins (genetics)</term>
<term>Repressor Proteins (metabolism)</term>
<term>Ribonucleoprotein, U2 Small Nuclear (antagonists & inhibitors)</term>
<term>Ribonucleoprotein, U2 Small Nuclear (genetics)</term>
<term>Ribonucleoprotein, U2 Small Nuclear (metabolism)</term>
<term>Sulfonamides (toxicity)</term>
<term>bcl-2 Homologous Antagonist-Killer Protein (metabolism)</term>
<term>bcl-2-Associated X Protein (metabolism)</term>
<term>bcl-X Protein (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Apoptose ()</term>
<term>Caspase-3 (métabolisme)</term>
<term>Caspase-7 (métabolisme)</term>
<term>Cellules HeLa</term>
<term>Dérivés du biphényle (toxicité)</term>
<term>Facteurs d'épissage des ARN</term>
<term>Humains</term>
<term>Interférence par ARN</term>
<term>Lignée cellulaire tumorale</term>
<term>Morpholines (toxicité)</term>
<term>Nitrophénols (toxicité)</term>
<term>Papillomavirus humain de type 16 (métabolisme)</term>
<term>Petit ARN interférent (métabolisme)</term>
<term>Petites ribonucléoprotéines nucléaires U2 (antagonistes et inhibiteurs)</term>
<term>Petites ribonucléoprotéines nucléaires U2 (génétique)</term>
<term>Petites ribonucléoprotéines nucléaires U2 (métabolisme)</term>
<term>Phosphoprotéines (antagonistes et inhibiteurs)</term>
<term>Phosphoprotéines (génétique)</term>
<term>Phosphoprotéines (métabolisme)</term>
<term>Pipérazines (toxicité)</term>
<term>Protéine Bak (métabolisme)</term>
<term>Protéine Bax (métabolisme)</term>
<term>Protéine Mcl-1 (génétique)</term>
<term>Protéine Mcl-1 (métabolisme)</term>
<term>Protéine bcl-X (métabolisme)</term>
<term>Protéines de répression (génétique)</term>
<term>Protéines de répression (métabolisme)</term>
<term>Protéines des oncogènes viraux (génétique)</term>
<term>Protéines des oncogènes viraux (métabolisme)</term>
<term>Pyrannes (toxicité)</term>
<term>Sulfonamides (toxicité)</term>
<term>Synergie des médicaments</term>
<term>Tumeurs de la tête et du cou (anatomopathologie)</term>
<term>Tumeurs de la tête et du cou (métabolisme)</term>
<term>Tumeurs de la tête et du cou (virologie)</term>
<term>Épissage des ARN ()</term>
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<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Phosphoproteins</term>
<term>Ribonucleoprotein, U2 Small Nuclear</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Myeloid Cell Leukemia Sequence 1 Protein</term>
<term>Oncogene Proteins, Viral</term>
<term>Phosphoproteins</term>
<term>Repressor Proteins</term>
<term>Ribonucleoprotein, U2 Small Nuclear</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Caspase 3</term>
<term>Caspase 7</term>
<term>Myeloid Cell Leukemia Sequence 1 Protein</term>
<term>Oncogene Proteins, Viral</term>
<term>Phosphoproteins</term>
<term>RNA, Small Interfering</term>
<term>Repressor Proteins</term>
<term>Ribonucleoprotein, U2 Small Nuclear</term>
<term>bcl-2 Homologous Antagonist-Killer Protein</term>
<term>bcl-2-Associated X Protein</term>
<term>bcl-X Protein</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Biphenyl Compounds</term>
<term>Morpholines</term>
<term>Nitrophenols</term>
<term>Piperazines</term>
<term>Pyrans</term>
<term>Sulfonamides</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Tumeurs de la tête et du cou</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Petites ribonucléoprotéines nucléaires U2</term>
<term>Phosphoprotéines</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term>
<term>RNA Splicing</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Petites ribonucléoprotéines nucléaires U2</term>
<term>Phosphoprotéines</term>
<term>Protéine Mcl-1</term>
<term>Protéines de répression</term>
<term>Protéines des oncogènes viraux</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Head and Neck Neoplasms</term>
<term>Human papillomavirus 16</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Caspase-3</term>
<term>Caspase-7</term>
<term>Papillomavirus humain de type 16</term>
<term>Petit ARN interférent</term>
<term>Petites ribonucléoprotéines nucléaires U2</term>
<term>Phosphoprotéines</term>
<term>Protéine Bak</term>
<term>Protéine Bax</term>
<term>Protéine Mcl-1</term>
<term>Protéine bcl-X</term>
<term>Protéines de répression</term>
<term>Protéines des oncogènes viraux</term>
<term>Tumeurs de la tête et du cou</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Head and Neck Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="toxicité" xml:lang="fr"><term>Dérivés du biphényle</term>
<term>Morpholines</term>
<term>Nitrophénols</term>
<term>Pipérazines</term>
<term>Pyrannes</term>
<term>Sulfonamides</term>
</keywords>
<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Tumeurs de la tête et du cou</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Head and Neck Neoplasms</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term>
<term>Drug Synergism</term>
<term>HeLa Cells</term>
<term>Humans</term>
<term>RNA Interference</term>
<term>RNA Splicing Factors</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Apoptose</term>
<term>Cellules HeLa</term>
<term>Facteurs d'épissage des ARN</term>
<term>Humains</term>
<term>Interférence par ARN</term>
<term>Lignée cellulaire tumorale</term>
<term>Synergie des médicaments</term>
<term>Épissage des ARN</term>
</keywords>
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<front><div type="abstract" xml:lang="en"><p>ABT-737 inhibits the anti-apoptotic proteins B-cell lymphoma 2 (BCL-2) and BCL-X<sub>L</sub>
. Meayamycin B switches the splicing pattern of myeloid cell leukemia factor 1 (MCL1) pre-mRNA. Specifically, inhibition of splicing factor 3B subunit 1 (SF3B1) with meayamycin B promotes the generation of the proapoptotic, short splicing variant (MCL1-S) and diminishes the antiapoptotic, long variant (MCL1-L). This action was previously associated with the cytotoxicity of meayamycin B in non-small cell lung carcinoma cell lines. ABT-737 induced apoptosis in response to an ablation of MCL1-L by meayamycin B. In this study, we further exploited this synergistic combination in head and neck squamous cell carcinoma (HNSCC), up to 90% of which overexpress MCL1 and BCL-X<sub>L</sub>
. In a panel of seven HNSCC cell lines, the combination of meayamycin B and ABT-737 rapidly triggered a Bax/Bak-mediated apoptosis that overcame the resistance from HPV16-positive HNSCC against each agent alone. Both RT-PCR and Western blotting showed that meayamycin B up-regulated MCL1-S and down-regulated MCL1-L. Significantly, we discovered that SF3B1 was involved in the splicing of oncogenic HPV16 E6 to produce non-oncogenic HPV16 E6*, indicating that SF3B1 may inhibit HPV16-induced tumorigenesis.</p>
</div>
</front>
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<biblStruct><analytic><author><name sortKey="Kreimer, A R" uniqKey="Kreimer A">A. R. Kreimer</name>
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<author><name sortKey="Clifford, G M" uniqKey="Clifford G">G. M. Clifford</name>
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<author><name sortKey="Boyle, P" uniqKey="Boyle P">P. Boyle</name>
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<author><name sortKey="Franceschi, S" uniqKey="Franceschi S">S. Franceschi</name>
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<biblStruct><analytic><author><name sortKey="Koutsky, L A" uniqKey="Koutsky L">L. A. Koutsky</name>
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<biblStruct><analytic><author><name sortKey="D Souza, G" uniqKey="D Souza G">G. D'souza</name>
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<biblStruct><analytic><author><name sortKey="Chaturvedi, A K" uniqKey="Chaturvedi A">A. K. Chaturvedi</name>
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<author><name sortKey="Engels, E A" uniqKey="Engels E">E. A. Engels</name>
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<author><name sortKey="Anderson, W F" uniqKey="Anderson W">W. F. Anderson</name>
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<biblStruct><analytic><author><name sortKey="Gillison, M L" uniqKey="Gillison M">M. L. Gillison</name>
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