GlutaredoxinV1, Main, Exploration, bibRecord, 000417

Selenite promotes all-trans retinoic acid-induced maturation of acute promyelocytic leukemia cells.

Identifieur interne : 000417 ( Main/Exploration ); précédent : 000416; suivant : 000418

Selenite promotes all-trans retinoic acid-induced maturation of acute promyelocytic leukemia cells.

Auteurs : Sougat Misra [Suède] ; Arun Kumar Selvam [Suède] ; Marita Wallenberg [Suède] ; Aditya Ambati [Suède] ; András Matolcsy [Hongrie] ; Isabelle Magalhaes [Suède] ; Gilbert Lauter [Suède] ; Mikael Björnstedt [Suède]

Source :

Oncotarget [ 1949-2553 ] ; 2016.

RBID : pubmed:27732960

Descripteurs français

English descriptors

KwdEn :
- Antineoplastic Agents (pharmacology), Cell Differentiation (drug effects), Cell Differentiation (genetics), Cell Line, Tumor (MeSH), Cell Proliferation (drug effects), Cell Survival (drug effects), Drug Synergism (MeSH), Gene Expression Regulation, Leukemic (drug effects), Glutaredoxins (genetics), Glutaredoxins (metabolism), Humans (MeSH), Leukemia, Promyelocytic, Acute (genetics), Leukemia, Promyelocytic, Acute (pathology), Oncogene Proteins, Fusion (genetics), Oncogene Proteins, Fusion (metabolism), Selenious Acid (pharmacology), Thioredoxins (genetics), Thioredoxins (metabolism), Transcription Factors (genetics), Transcription Factors (metabolism), Tretinoin (pharmacology), Tumor Cells, Cultured (MeSH).
MESH :
- chemical , genetics : Glutaredoxins, Oncogene Proteins, Fusion, Thioredoxins, Transcription Factors.
- chemical , metabolism : Glutaredoxins, Oncogene Proteins, Fusion, Thioredoxins, Transcription Factors.
- chemical , pharmacology : Antineoplastic Agents, Selenious Acid, Tretinoin.
- drug effects : Cell Differentiation, Cell Proliferation, Cell Survival, Gene Expression Regulation, Leukemic.
- genetics : Cell Differentiation, Leukemia, Promyelocytic, Acute.
- pathology : Leukemia, Promyelocytic, Acute.
- Cell Line, Tumor, Drug Synergism, Humans, Tumor Cells, Cultured.

Abstract

Selective targeting of the PML/RARα oncoprotein demonstrates a successful molecular targeted therapy in acute promyelocytic leukemia (APL) with a typical t(15:17) chromosomal translocation. The zinc-thiolate coordination is critical for structural stability of zinc finger proteins, including the PML moiety of PML/RARα. Based on the known interaction of redox-active selenium compounds with thiolate ligands of zinc, we herein have investigated the abrogatory effects of selenite alone or in combination with all-trans retinoic acid on PML/RARα and the possible effects on differentiation in these cells. At pharmacological concentrations, selenite inhibited the proliferation and survival of APL originated NB4 cells. In combination with ATRA, it potentiated the differentiation of NB4 cells without any differentiating effects of its own as a single agent. Concordant with our hypothesis, PML/RARα oncoprotein expression was completely abrogated by selenite. Increased expression of RARα, PU.1 and FOXO3A transcription factors in the combined treatment suggested the plausible basis for increased differentiation in these cells. We show that selenite at clinically achievable dose targets PML/RARα oncoprotein for degradation and potentiates differentiation of promyelocytic leukemic cells in combination with ATRA. The present investigation reveals the hitherto unknown potential of selenite in targeted abrogation of PML/RARα in APL cells with prospective therapeutic value.

DOI: 10.18632/oncotarget.12531
PubMed: 27732960
PubMed Central: PMC5342695

Affiliations:

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Le document en format XML

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<term>Cell Differentiation (drug effects)</term>
<term>Cell Differentiation (genetics)</term>
<term>Cell Line, Tumor (MeSH)</term>
<term>Cell Proliferation (drug effects)</term>
<term>Cell Survival (drug effects)</term>
<term>Drug Synergism (MeSH)</term>
<term>Gene Expression Regulation, Leukemic (drug effects)</term>
<term>Glutaredoxins (genetics)</term>
<term>Glutaredoxins (metabolism)</term>
<term>Humans (MeSH)</term>
<term>Leukemia, Promyelocytic, Acute (genetics)</term>
<term>Leukemia, Promyelocytic, Acute (pathology)</term>
<term>Oncogene Proteins, Fusion (genetics)</term>
<term>Oncogene Proteins, Fusion (metabolism)</term>
<term>Selenious Acid (pharmacology)</term>
<term>Thioredoxins (genetics)</term>
<term>Thioredoxins (metabolism)</term>
<term>Transcription Factors (genetics)</term>
<term>Transcription Factors (metabolism)</term>
<term>Tretinoin (pharmacology)</term>
<term>Tumor Cells, Cultured (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Acide sélénieux (pharmacologie)</term>
<term>Antinéoplasiques (pharmacologie)</term>
<term>Cellules cancéreuses en culture (MeSH)</term>
<term>Différenciation cellulaire (effets des médicaments et des substances chimiques)</term>
<term>Différenciation cellulaire (génétique)</term>
<term>Facteurs de transcription (génétique)</term>
<term>Facteurs de transcription (métabolisme)</term>
<term>Glutarédoxines (génétique)</term>
<term>Glutarédoxines (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Leucémie aiguë promyélocytaire (anatomopathologie)</term>
<term>Leucémie aiguë promyélocytaire (génétique)</term>
<term>Lignée cellulaire tumorale (MeSH)</term>
<term>Prolifération cellulaire (effets des médicaments et des substances chimiques)</term>
<term>Protéines de fusion oncogènes (génétique)</term>
<term>Protéines de fusion oncogènes (métabolisme)</term>
<term>Régulation de l'expression des gènes dans la leucémie (effets des médicaments et des substances chimiques)</term>
<term>Survie cellulaire (effets des médicaments et des substances chimiques)</term>
<term>Synergie des médicaments (MeSH)</term>
<term>Thiorédoxines (génétique)</term>
<term>Thiorédoxines (métabolisme)</term>
<term>Trétinoïne (pharmacologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glutaredoxins</term>
<term>Oncogene Proteins, Fusion</term>
<term>Thioredoxins</term>
<term>Transcription Factors</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glutaredoxins</term>
<term>Oncogene Proteins, Fusion</term>
<term>Thioredoxins</term>
<term>Transcription Factors</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Agents</term>
<term>Selenious Acid</term>
<term>Tretinoin</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Leucémie aiguë promyélocytaire</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Differentiation</term>
<term>Cell Proliferation</term>
<term>Cell Survival</term>
<term>Gene Expression Regulation, Leukemic</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Différenciation cellulaire</term>
<term>Prolifération cellulaire</term>
<term>Régulation de l'expression des gènes dans la leucémie</term>
<term>Survie cellulaire</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cell Differentiation</term>
<term>Leukemia, Promyelocytic, Acute</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Différenciation cellulaire</term>
<term>Facteurs de transcription</term>
<term>Glutarédoxines</term>
<term>Leucémie aiguë promyélocytaire</term>
<term>Protéines de fusion oncogènes</term>
<term>Thiorédoxines</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteurs de transcription</term>
<term>Glutarédoxines</term>
<term>Protéines de fusion oncogènes</term>
<term>Thiorédoxines</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Leukemia, Promyelocytic, Acute</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Acide sélénieux</term>
<term>Antinéoplasiques</term>
<term>Trétinoïne</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term>
<term>Drug Synergism</term>
<term>Humans</term>
<term>Tumor Cells, Cultured</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Cellules cancéreuses en culture</term>
<term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Synergie des médicaments</term>
</keywords>
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<front><div type="abstract" xml:lang="en">Selective targeting of the PML/RARα oncoprotein demonstrates a successful molecular targeted therapy in acute promyelocytic leukemia (APL) with a typical t(15:17) chromosomal translocation. The zinc-thiolate coordination is critical for structural stability of zinc finger proteins, including the PML moiety of PML/RARα. Based on the known interaction of redox-active selenium compounds with thiolate ligands of zinc, we herein have investigated the abrogatory effects of selenite alone or in combination with all-trans retinoic acid on PML/RARα and the possible effects on differentiation in these cells. At pharmacological concentrations, selenite inhibited the proliferation and survival of APL originated NB4 cells. In combination with ATRA, it potentiated the differentiation of NB4 cells without any differentiating effects of its own as a single agent. Concordant with our hypothesis, PML/RARα oncoprotein expression was completely abrogated by selenite. Increased expression of  RARα, PU.1 and FOXO3A transcription factors in the combined treatment suggested the plausible basis for increased differentiation in these cells. We show that selenite at clinically achievable dose targets PML/RARα oncoprotein for degradation and potentiates differentiation of promyelocytic leukemic cells in combination with ATRA. The present investigation reveals the hitherto unknown potential of selenite in targeted abrogation of PML/RARα in APL cells with prospective therapeutic value.</div>
</front>
</TEI>
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<DateCompleted><Year>2018</Year>
<Month>02</Month>
<Day>26</Day>
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<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
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<Issue>46</Issue>
<PubDate><Year>2016</Year>
<Month>11</Month>
<Day>15</Day>
</PubDate>
</JournalIssue>
<Title>Oncotarget</Title>
<ISOAbbreviation>Oncotarget</ISOAbbreviation>
</Journal>
<ArticleTitle>Selenite promotes all-trans retinoic acid-induced maturation of acute promyelocytic leukemia cells.</ArticleTitle>
<Pagination><MedlinePgn>74686-74700</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.18632/oncotarget.12531</ELocationID>
<Abstract><AbstractText>Selective targeting of the PML/RARα oncoprotein demonstrates a successful molecular targeted therapy in acute promyelocytic leukemia (APL) with a typical t(15:17) chromosomal translocation. The zinc-thiolate coordination is critical for structural stability of zinc finger proteins, including the PML moiety of PML/RARα. Based on the known interaction of redox-active selenium compounds with thiolate ligands of zinc, we herein have investigated the abrogatory effects of selenite alone or in combination with all-trans retinoic acid on PML/RARα and the possible effects on differentiation in these cells. At pharmacological concentrations, selenite inhibited the proliferation and survival of APL originated NB4 cells. In combination with ATRA, it potentiated the differentiation of NB4 cells without any differentiating effects of its own as a single agent. Concordant with our hypothesis, PML/RARα oncoprotein expression was completely abrogated by selenite. Increased expression of  RARα, PU.1 and FOXO3A transcription factors in the combined treatment suggested the plausible basis for increased differentiation in these cells. We show that selenite at clinically achievable dose targets PML/RARα oncoprotein for degradation and potentiates differentiation of promyelocytic leukemic cells in combination with ATRA. The present investigation reveals the hitherto unknown potential of selenite in targeted abrogation of PML/RARα in APL cells with prospective therapeutic value.</AbstractText>
</Abstract>
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<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Laboratory Medicine, Division of Pathology F46, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Selvam</LastName>
<ForeName>Arun Kumar</ForeName>
<Initials>AK</Initials>
<AffiliationInfo><Affiliation>Department of Laboratory Medicine, Division of Pathology F46, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.</Affiliation>
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Selenite promotes all-trans retinoic acid-induced maturation of acute promyelocytic leukemia cells.

Selenite promotes all-trans retinoic acid-induced maturation of acute promyelocytic leukemia cells.

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