RapamycinFungusV1, Main, Exploration, bibRecord, 000960

eIF4B is a convergent target and critical effector of oncogenic Pim and PI3K/Akt/mTOR signaling pathways in Abl transformants.

Identifieur interne : 000960 ( Main/Exploration ); précédent : 000959; suivant : 000961

eIF4B is a convergent target and critical effector of oncogenic Pim and PI3K/Akt/mTOR signaling pathways in Abl transformants.

Auteurs : Ke Chen [République populaire de Chine] ; Jianling Yang [République populaire de Chine] ; Jianning Li [République populaire de Chine] ; Xuefei Wang [République populaire de Chine] ; Yuhai Chen [République populaire de Chine] ; Shile Huang [États-Unis] ; Ji-Long Chen [République populaire de Chine]

Source :

Oncotarget [ 1949-2553 ] ; 2016.

RBID : pubmed:26848623

Descripteurs français

English descriptors

Abstract

Activation of eIF4B correlates with Abl-mediated cellular transformation, but the precise mechanisms are largely unknown. Here we show that eIF4B is a convergent substrate of JAK/STAT/Pim and PI3K/Akt/mTOR pathways in Abl transformants. Both pathways phosphorylated eIF4B in Abl-transformed cells, and such redundant regulation was responsible for the limited effect of single inhibitor on Abl oncogenicity. Persistent inhibition of one signaling pathway induced the activation of the other pathway and thereby restored the phosphorylation levels of eIF4B. Simultaneous inhibition of the two pathways impaired eIF4B phosphorylation more effectively, and synergistically induced apoptosis in Abl transformed cells and inhibited the growth of engrafted tumors in nude mice. Similarly, the survival of Abl transformants exhibited a higher sensitivity to the pharmacological inhibition, when combined with the shRNA-based silence of the other pathway. Interestingly, such synergy was dependent on the phosphorylation status of eIF4B on Ser422, as overexpression of eIF4B phosphomimetic mutant S422E in the transformants greatly attenuated the synergistic effects of these inhibitors on Abl oncogenicity. In contrast, eIF4B knockdown sensitized Abl transformants to undergo apoptosis induced by the combined blockage. Collectively, the results indicate that eIF4B integrates the signals from Pim and PI3K/Akt/mTOR pathways in Abl-expressing leukemic cells, and is a promising therapeutic target for such cancers.

DOI: 10.18632/oncotarget.7164
PubMed: 26848623
PubMed Central: PMC4891105

Affiliations:

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<term>Antibiotics, Antineoplastic (pharmacology)</term>
<term>Blotting, Western (MeSH)</term>
<term>Cell Line (MeSH)</term>
<term>Cell Survival (drug effects)</term>
<term>Cell Survival (genetics)</term>
<term>Cell Transformation, Neoplastic (genetics)</term>
<term>Cell Transformation, Neoplastic (metabolism)</term>
<term>Enzyme Inhibitors (pharmacology)</term>
<term>Eukaryotic Initiation Factors (genetics)</term>
<term>Eukaryotic Initiation Factors (metabolism)</term>
<term>HEK293 Cells (MeSH)</term>
<term>Humans (MeSH)</term>
<term>K562 Cells (MeSH)</term>
<term>Leukemia, Experimental (drug therapy)</term>
<term>Leukemia, Experimental (genetics)</term>
<term>Leukemia, Experimental (metabolism)</term>
<term>Mice, Inbred BALB C (MeSH)</term>
<term>Mice, Nude (MeSH)</term>
<term>Phosphatidylinositol 3-Kinases (genetics)</term>
<term>Phosphatidylinositol 3-Kinases (metabolism)</term>
<term>Phosphoinositide-3 Kinase Inhibitors (MeSH)</term>
<term>Phosphorylation (drug effects)</term>
<term>Proto-Oncogene Proteins c-abl (genetics)</term>
<term>Proto-Oncogene Proteins c-abl (metabolism)</term>
<term>Proto-Oncogene Proteins c-akt (antagonists & inhibitors)</term>
<term>Proto-Oncogene Proteins c-akt (genetics)</term>
<term>Proto-Oncogene Proteins c-akt (metabolism)</term>
<term>Proto-Oncogene Proteins c-pim-1 (antagonists & inhibitors)</term>
<term>Proto-Oncogene Proteins c-pim-1 (genetics)</term>
<term>Proto-Oncogene Proteins c-pim-1 (metabolism)</term>
<term>RNA Interference (MeSH)</term>
<term>Signal Transduction (drug effects)</term>
<term>Signal Transduction (genetics)</term>
<term>Sirolimus (pharmacology)</term>
<term>TOR Serine-Threonine Kinases (antagonists & inhibitors)</term>
<term>TOR Serine-Threonine Kinases (genetics)</term>
<term>TOR Serine-Threonine Kinases (metabolism)</term>
<term>Tumor Burden (drug effects)</term>
<term>Xenograft Model Antitumor Assays (MeSH)</term>
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<term>Antibiotiques antinéoplasiques (pharmacologie)</term>
<term>Antienzymes (pharmacologie)</term>
<term>Cellules HEK293 (MeSH)</term>
<term>Cellules K562 (MeSH)</term>
<term>Charge tumorale (effets des médicaments et des substances chimiques)</term>
<term>Facteurs d'initiation eucaryotes (génétique)</term>
<term>Facteurs d'initiation eucaryotes (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Interférence par ARN (MeSH)</term>
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<term>Leucémie expérimentale (métabolisme)</term>
<term>Leucémie expérimentale (traitement médicamenteux)</term>
<term>Lignée cellulaire (MeSH)</term>
<term>Phosphatidylinositol 3-kinases (génétique)</term>
<term>Phosphatidylinositol 3-kinases (métabolisme)</term>
<term>Phosphorylation (effets des médicaments et des substances chimiques)</term>
<term>Protéines proto-oncogènes c-abl (génétique)</term>
<term>Protéines proto-oncogènes c-abl (métabolisme)</term>
<term>Protéines proto-oncogènes c-akt (antagonistes et inhibiteurs)</term>
<term>Protéines proto-oncogènes c-akt (génétique)</term>
<term>Protéines proto-oncogènes c-akt (métabolisme)</term>
<term>Protéines proto-oncogènes c-pim-1 (antagonistes et inhibiteurs)</term>
<term>Protéines proto-oncogènes c-pim-1 (génétique)</term>
<term>Protéines proto-oncogènes c-pim-1 (métabolisme)</term>
<term>Sirolimus (pharmacologie)</term>
<term>Souris de lignée BALB C (MeSH)</term>
<term>Souris nude (MeSH)</term>
<term>Survie cellulaire (effets des médicaments et des substances chimiques)</term>
<term>Survie cellulaire (génétique)</term>
<term>Sérine-thréonine kinases TOR (antagonistes et inhibiteurs)</term>
<term>Sérine-thréonine kinases TOR (génétique)</term>
<term>Sérine-thréonine kinases TOR (métabolisme)</term>
<term>Technique de Western (MeSH)</term>
<term>Tests d'activité antitumorale sur modèle de xénogreffe (MeSH)</term>
<term>Transduction du signal (effets des médicaments et des substances chimiques)</term>
<term>Transduction du signal (génétique)</term>
<term>Transformation cellulaire néoplasique (génétique)</term>
<term>Transformation cellulaire néoplasique (métabolisme)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Proto-Oncogene Proteins c-akt</term>
<term>Proto-Oncogene Proteins c-pim-1</term>
<term>TOR Serine-Threonine Kinases</term>
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<term>Proto-Oncogene Proteins c-abl</term>
<term>Proto-Oncogene Proteins c-akt</term>
<term>Proto-Oncogene Proteins c-pim-1</term>
<term>TOR Serine-Threonine Kinases</term>
</keywords>
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<term>Proto-Oncogene Proteins c-abl</term>
<term>Proto-Oncogene Proteins c-akt</term>
<term>Proto-Oncogene Proteins c-pim-1</term>
<term>TOR Serine-Threonine Kinases</term>
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<term>Enzyme Inhibitors</term>
<term>Sirolimus</term>
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<term>Protéines proto-oncogènes c-pim-1</term>
<term>Sérine-thréonine kinases TOR</term>
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<term>Phosphorylation</term>
<term>Signal Transduction</term>
<term>Tumor Burden</term>
</keywords>
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</keywords>
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<term>Phosphorylation</term>
<term>Survie cellulaire</term>
<term>Transduction du signal</term>
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<term>Leukemia, Experimental</term>
<term>Phosphatidylinositol 3-Kinases</term>
<term>Signal Transduction</term>
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<term>Leucémie expérimentale</term>
<term>Phosphatidylinositol 3-kinases</term>
<term>Protéines proto-oncogènes c-abl</term>
<term>Protéines proto-oncogènes c-akt</term>
<term>Protéines proto-oncogènes c-pim-1</term>
<term>Survie cellulaire</term>
<term>Sérine-thréonine kinases TOR</term>
<term>Transduction du signal</term>
<term>Transformation cellulaire néoplasique</term>
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<term>Leukemia, Experimental</term>
<term>Phosphatidylinositol 3-Kinases</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteurs d'initiation eucaryotes</term>
<term>Leucémie expérimentale</term>
<term>Phosphatidylinositol 3-kinases</term>
<term>Protéines proto-oncogènes c-abl</term>
<term>Protéines proto-oncogènes c-akt</term>
<term>Protéines proto-oncogènes c-pim-1</term>
<term>Sérine-thréonine kinases TOR</term>
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<term>Antienzymes</term>
<term>Sirolimus</term>
</keywords>
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</keywords>
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<term>Blotting, Western</term>
<term>Cell Line</term>
<term>HEK293 Cells</term>
<term>Humans</term>
<term>K562 Cells</term>
<term>Mice, Inbred BALB C</term>
<term>Mice, Nude</term>
<term>Phosphoinositide-3 Kinase Inhibitors</term>
<term>RNA Interference</term>
<term>Xenograft Model Antitumor Assays</term>
</keywords>
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<term>Cellules HEK293</term>
<term>Cellules K562</term>
<term>Humains</term>
<term>Interférence par ARN</term>
<term>Lignée cellulaire</term>
<term>Souris de lignée BALB C</term>
<term>Souris nude</term>
<term>Technique de Western</term>
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<front><div type="abstract" xml:lang="en">Activation of eIF4B correlates with Abl-mediated cellular transformation, but the precise mechanisms are largely unknown. Here we show that eIF4B is a convergent substrate of JAK/STAT/Pim and PI3K/Akt/mTOR pathways in Abl transformants. Both pathways phosphorylated eIF4B in Abl-transformed cells, and such redundant regulation was responsible for the limited effect of single inhibitor on Abl oncogenicity. Persistent inhibition of one signaling pathway induced the activation of the other pathway and thereby restored the phosphorylation levels of eIF4B. Simultaneous inhibition of the two pathways impaired eIF4B phosphorylation more effectively, and synergistically induced apoptosis in Abl transformed cells and inhibited the growth of engrafted tumors in nude mice. Similarly, the survival of Abl transformants exhibited a higher sensitivity to the pharmacological inhibition, when combined with the shRNA-based silence of the other pathway. Interestingly, such synergy was dependent on the phosphorylation status of eIF4B on Ser422, as overexpression of eIF4B phosphomimetic mutant S422E in the transformants greatly attenuated the synergistic effects of these inhibitors on Abl oncogenicity. In contrast, eIF4B knockdown sensitized Abl transformants to undergo apoptosis induced by the combined blockage. Collectively, the results indicate that eIF4B integrates the signals from Pim and PI3K/Akt/mTOR pathways in Abl-expressing leukemic cells, and is a promising therapeutic target for such cancers. </div>
</front>
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<DateCompleted><Year>2017</Year>
<Month>01</Month>
<Day>16</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>12</Month>
<Day>10</Day>
</DateRevised>
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<JournalIssue CitedMedium="Internet"><Volume>7</Volume>
<Issue>9</Issue>
<PubDate><Year>2016</Year>
<Month>Mar</Month>
<Day>01</Day>
</PubDate>
</JournalIssue>
<Title>Oncotarget</Title>
<ISOAbbreviation>Oncotarget</ISOAbbreviation>
</Journal>
<ArticleTitle>eIF4B is a convergent target and critical effector of oncogenic Pim and PI3K/Akt/mTOR signaling pathways in Abl transformants.</ArticleTitle>
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<Abstract><AbstractText>Activation of eIF4B correlates with Abl-mediated cellular transformation, but the precise mechanisms are largely unknown. Here we show that eIF4B is a convergent substrate of JAK/STAT/Pim and PI3K/Akt/mTOR pathways in Abl transformants. Both pathways phosphorylated eIF4B in Abl-transformed cells, and such redundant regulation was responsible for the limited effect of single inhibitor on Abl oncogenicity. Persistent inhibition of one signaling pathway induced the activation of the other pathway and thereby restored the phosphorylation levels of eIF4B. Simultaneous inhibition of the two pathways impaired eIF4B phosphorylation more effectively, and synergistically induced apoptosis in Abl transformed cells and inhibited the growth of engrafted tumors in nude mice. Similarly, the survival of Abl transformants exhibited a higher sensitivity to the pharmacological inhibition, when combined with the shRNA-based silence of the other pathway. Interestingly, such synergy was dependent on the phosphorylation status of eIF4B on Ser422, as overexpression of eIF4B phosphomimetic mutant S422E in the transformants greatly attenuated the synergistic effects of these inhibitors on Abl oncogenicity. In contrast, eIF4B knockdown sensitized Abl transformants to undergo apoptosis induced by the combined blockage. Collectively, the results indicate that eIF4B integrates the signals from Pim and PI3K/Akt/mTOR pathways in Abl-expressing leukemic cells, and is a promising therapeutic target for such cancers. </AbstractText>
</Abstract>
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<ForeName>Ke</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing 100101, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yang</LastName>
<ForeName>Jianling</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing 100101, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Key Laboratory of Immune Mechanism and Intervention on Serious Disease in Hebei Province, Department of Immunology, Hebei Medical University, Shijiazhuang 050017, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Jianning</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing 100101, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Xuefei</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing 100101, China.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Yuhai</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing 100101, China.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Huang</LastName>
<ForeName>Shile</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry and Molecular Biology, Louisiana State University Health Sciences Center, Shreveport, LA 71130, USA.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Ji-Long</ForeName>
<Initials>JL</Initials>
<AffiliationInfo><Affiliation>CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing 100101, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>College of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou 350002, China.</Affiliation>
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<name sortKey="Li, Jianning" sort="Li, Jianning" uniqKey="Li J" first="Jianning" last="Li">Jianning Li</name>
<name sortKey="Wang, Xuefei" sort="Wang, Xuefei" uniqKey="Wang X" first="Xuefei" last="Wang">Xuefei Wang</name>
<name sortKey="Yang, Jianling" sort="Yang, Jianling" uniqKey="Yang J" first="Jianling" last="Yang">Jianling Yang</name>
<name sortKey="Yang, Jianling" sort="Yang, Jianling" uniqKey="Yang J" first="Jianling" last="Yang">Jianling Yang</name>
</country>
<country name="États-Unis"><region name="Louisiane"><name sortKey="Huang, Shile" sort="Huang, Shile" uniqKey="Huang S" first="Shile" last="Huang">Shile Huang</name>
</region>
</country>
</tree>
</affiliations>
</record>

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HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000960 | SxmlIndent | more

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Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Bois
   |area=    RapamycinFungusV1
   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     pubmed:26848623
   |texte=   eIF4B is a convergent target and critical effector of oncogenic Pim and PI3K/Akt/mTOR signaling pathways in Abl transformants.
}}

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       | NlmPubMed2Wicri -a RapamycinFungusV1

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	Serveur d'exploration sur la rapamycine et les champignons
	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 sur la rapamycine et les champignons

eIF4B is a convergent target and critical effector of oncogenic Pim and PI3K/Akt/mTOR signaling pathways in Abl transformants.

eIF4B is a convergent target and critical effector of oncogenic Pim and PI3K/Akt/mTOR signaling pathways in Abl transformants.

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