C16‑ceramide and sphingosine 1‑phosphate/S1PR2 have opposite effects on cell growth through mTOR signaling pathway regulation.
Identifieur interne : 000645 ( Main/Exploration ); précédent : 000644; suivant : 000646C16‑ceramide and sphingosine 1‑phosphate/S1PR2 have opposite effects on cell growth through mTOR signaling pathway regulation.
Auteurs : Min Hee Kim [Corée du Sud] ; Joo-Won Park [Corée du Sud] ; Eun-Ji Lee [Corée du Sud] ; Shin Kim [Corée du Sud] ; Sun-Hye Shin [Corée du Sud] ; Jung-Hyuck Ahn [Corée du Sud] ; Yunjae Jung [Corée du Sud] ; Inkeun Park [Corée du Sud] ; Woo-Jae Park [Corée du Sud]Source :
- Oncology reports [ 1791-2431 ] ; 2018.
Descripteurs français
- KwdFr :
- Cellules MCF-7 (MeSH), Céramides (biosynthèse), Céramides (génétique), Femelle (MeSH), Humains (MeSH), Lysophospholipides (biosynthèse), Lysophospholipides (génétique), Morpholines (pharmacologie), Phosphorylation (MeSH), Phosphotransferases (Alcohol Group Acceptor) (antagonistes et inhibiteurs), Phosphotransferases (Alcohol Group Acceptor) (génétique), Prolifération cellulaire (génétique), Protéine oncogène v-akt (génétique), Protéines membranaires (génétique), Récepteurs aux lysosphingolipides (antagonistes et inhibiteurs), Récepteurs aux lysosphingolipides (génétique), Régulation de l'expression des gènes tumoraux (MeSH), Sphingosine (analogues et dérivés), Sphingosine (biosynthèse), Sphingosine (génétique), Sphingosine N-acyltransferase (génétique), Système de signalisation des MAP kinases (effets des médicaments et des substances chimiques), Sérine-thréonine kinases TOR (génétique), Transduction du signal (effets des médicaments et des substances chimiques), Triazines (pharmacologie), Tumeurs du sein (anatomopathologie), Tumeurs du sein (génétique).
- MESH :
- analogues et dérivés : Sphingosine.
- anatomopathologie : Tumeurs du sein.
- antagonistes et inhibiteurs : Phosphotransferases (Alcohol Group Acceptor), Récepteurs aux lysosphingolipides.
- biosynthèse : Céramides, Lysophospholipides, Sphingosine.
- effets des médicaments et des substances chimiques : Système de signalisation des MAP kinases, Transduction du signal.
- génétique : Céramides, Lysophospholipides, Phosphotransferases (Alcohol Group Acceptor), Prolifération cellulaire, Protéine oncogène v-akt, Protéines membranaires, Récepteurs aux lysosphingolipides, Sphingosine, Sphingosine N-acyltransferase, Sérine-thréonine kinases TOR, Tumeurs du sein.
- pharmacologie : Morpholines, Triazines.
- Cellules MCF-7, Femelle, Humains, Phosphorylation, Régulation de l'expression des gènes tumoraux.
English descriptors
- KwdEn :
- Breast Neoplasms (genetics), Breast Neoplasms (pathology), Cell Proliferation (genetics), Ceramides (biosynthesis), Ceramides (genetics), Female (MeSH), Gene Expression Regulation, Neoplastic (MeSH), Humans (MeSH), Lysophospholipids (biosynthesis), Lysophospholipids (genetics), MAP Kinase Signaling System (drug effects), MCF-7 Cells (MeSH), Membrane Proteins (genetics), Morpholines (pharmacology), Oncogene Protein v-akt (genetics), Phosphorylation (MeSH), Phosphotransferases (Alcohol Group Acceptor) (antagonists & inhibitors), Phosphotransferases (Alcohol Group Acceptor) (genetics), Receptors, Lysosphingolipid (antagonists & inhibitors), Receptors, Lysosphingolipid (genetics), Signal Transduction (drug effects), Sphingosine (analogs & derivatives), Sphingosine (biosynthesis), Sphingosine (genetics), Sphingosine N-Acyltransferase (genetics), Sphingosine-1-Phosphate Receptors (MeSH), TOR Serine-Threonine Kinases (genetics), Triazines (pharmacology).
- MESH :
- chemical , analogs & derivatives : Sphingosine.
- chemical , antagonists & inhibitors : Phosphotransferases (Alcohol Group Acceptor), Receptors, Lysosphingolipid.
- chemical , biosynthesis : Ceramides, Lysophospholipids, Sphingosine.
- drug effects : MAP Kinase Signaling System, Signal Transduction.
- genetics : Breast Neoplasms, Cell Proliferation, Ceramides, Lysophospholipids, Membrane Proteins, Oncogene Protein v-akt, Phosphotransferases (Alcohol Group Acceptor), Receptors, Lysosphingolipid, Sphingosine, Sphingosine N-Acyltransferase, TOR Serine-Threonine Kinases.
- pathology : Breast Neoplasms.
- chemical , pharmacology : Morpholines, Triazines.
- Female, Gene Expression Regulation, Neoplastic, Humans, MCF-7 Cells, Phosphorylation, Sphingosine-1-Phosphate Receptors.
Abstract
Recently, sphingolipid derivatives, such as ceramide and sphingosine‑1‑phosphate (S1P), have emerged as key modulators in apoptotic cell death and cell proliferation. This study aimed to clarify the underlying signaling pathways of ceramide and S1P involved in breast cancer cell proliferation. Ceramide acyl chain length is determined by six mammalian ceramide synthases (CerS). We overexpressed CerS1 to 6 in MCF‑7 cells to examine whether ceramide signaling propagation varies as a function of acyl chain length. Among the six CerS, only CerS6 overexpression reduced phosphorylation of Akt, S6 kinase (S6K), and extracellular signal‑regulated kinases (ERK) as shown by western blotting. In addition, CerS6 overexpression reduced MCF‑7 cell proliferation. This effect was partially reversed by co‑treatment with MHY1485, an activator of mammalian target of rapamycin (mTOR), demonstrating an important role for the mTOR pathway in the CerS6‑mediated decrease in MCF‑7 cell proliferation. ERK inhibition, but not Akt inhibition, along with mTOR inhibition synergistically reduced MCF‑7 cell proliferation as measured by MTT assay. Notably, the expression of CerS6 and S1P receptor 2 (S1PR2), or CerS6 and sphingosine kinase 1 (SphK1), were negatively correlated according to the invasive breast carcinoma patient cohort in The Cancer Genome Atlas database. In addition, both SphK1 overexpression and S1P addition increased mTOR phosphorylation as shown by ELISA, while S1PR2 inhibition had the inverse effect. These data suggest that CerS6 and SphK1 regulate mTOR signaling in breast cancer cell proliferation. Moreover, mTOR activity can be regulated by the balance between S1P and C16‑ceramide, which is generated by CerS6.
DOI: 10.3892/or.2018.6689
PubMed: 30226616
Affiliations:
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wicri:level="1"><nlm:affiliation>Department of Immunology, School of Medicine, Keimyung University, Daegu 42601, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Immunology, School of Medicine, Keimyung University, Daegu 42601</wicri:regionArea><wicri:noRegion>Daegu 42601</wicri:noRegion></affiliation></author><author><name sortKey="Shin, Sun Hye" sort="Shin, Sun Hye" uniqKey="Shin S" first="Sun-Hye" last="Shin">Sun-Hye Shin</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry, College of Medicine, Ewha Womans University, Seoul 07985, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Biochemistry, College of Medicine, Ewha Womans University, Seoul 07985</wicri:regionArea><placeName><settlement type="city">Séoul</settlement><region type="capital">Région capitale de Séoul</region></placeName></affiliation></author><author><name 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sort="Park, Woo Jae" uniqKey="Park W" first="Woo-Jae" last="Park">Woo-Jae Park</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry, College of Medicine, Gachon University, Incheon 21999, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Biochemistry, College of Medicine, Gachon University, Incheon 21999</wicri:regionArea><wicri:noRegion>Incheon 21999</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2018">2018</date><idno type="RBID">pubmed:30226616</idno><idno type="pmid">30226616</idno><idno type="doi">10.3892/or.2018.6689</idno><idno type="wicri:Area/Main/Corpus">000453</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000453</idno><idno type="wicri:Area/Main/Curation">000453</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000453</idno><idno 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University, Seoul 07985, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Biochemistry, College of Medicine, Ewha Womans University, Seoul 07985</wicri:regionArea><placeName><settlement type="city">Séoul</settlement><region type="capital">Région capitale de Séoul</region></placeName></affiliation></author><author><name sortKey="Lee, Eun Ji" sort="Lee, Eun Ji" uniqKey="Lee E" first="Eun-Ji" last="Lee">Eun-Ji Lee</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry, College of Medicine, Gachon University, Incheon 21999, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Biochemistry, College of Medicine, Gachon University, Incheon 21999</wicri:regionArea><wicri:noRegion>Incheon 21999</wicri:noRegion></affiliation></author><author><name sortKey="Kim, Shin" sort="Kim, Shin" uniqKey="Kim S" first="Shin" last="Kim">Shin Kim</name><affiliation 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sortKey="Ahn, Jung Hyuck" sort="Ahn, Jung Hyuck" uniqKey="Ahn J" first="Jung-Hyuck" last="Ahn">Jung-Hyuck Ahn</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry, College of Medicine, Ewha Womans University, Seoul 07985, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Biochemistry, College of Medicine, Ewha Womans University, Seoul 07985</wicri:regionArea><placeName><settlement type="city">Séoul</settlement><region type="capital">Région capitale de Séoul</region></placeName></affiliation></author><author><name sortKey="Jung, Yunjae" sort="Jung, Yunjae" uniqKey="Jung Y" first="Yunjae" last="Jung">Yunjae Jung</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology, College of Medicine, Gachon University, Incheon 21999, Division of Medical Oncology, Department of Internal Medicine, Gachon University Gil Medical Center, Incheon 21565, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Microbiology, College of Medicine, Gachon University, Incheon 21999, Division of Medical Oncology, Department of Internal Medicine, Gachon University Gil Medical Center, Incheon 21565</wicri:regionArea><wicri:noRegion>Incheon 21565</wicri:noRegion></affiliation></author><author><name sortKey="Park, Inkeun" sort="Park, Inkeun" uniqKey="Park I" first="Inkeun" last="Park">Inkeun Park</name><affiliation wicri:level="1"><nlm:affiliation>Division of Medical Oncology, Department of Internal Medicine, Gachon University Gil Medical Center, Incheon 21565, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Division of Medical Oncology, Department of Internal Medicine, Gachon University Gil Medical Center, Incheon 21565</wicri:regionArea><wicri:noRegion>Incheon 21565</wicri:noRegion></affiliation></author><author><name sortKey="Park, Woo Jae" sort="Park, Woo Jae" uniqKey="Park W" first="Woo-Jae" last="Park">Woo-Jae Park</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry, College of Medicine, Gachon University, Incheon 21999, Republic of Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Biochemistry, College of Medicine, Gachon University, Incheon 21999</wicri:regionArea><wicri:noRegion>Incheon 21999</wicri:noRegion></affiliation></author></analytic><series><title level="j">Oncology reports</title><idno type="eISSN">1791-2431</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Breast Neoplasms (genetics)</term><term>Breast Neoplasms (pathology)</term><term>Cell Proliferation (genetics)</term><term>Ceramides (biosynthesis)</term><term>Ceramides (genetics)</term><term>Female (MeSH)</term><term>Gene Expression Regulation, Neoplastic (MeSH)</term><term>Humans (MeSH)</term><term>Lysophospholipids (biosynthesis)</term><term>Lysophospholipids (genetics)</term><term>MAP Kinase Signaling System (drug effects)</term><term>MCF-7 Cells (MeSH)</term><term>Membrane Proteins (genetics)</term><term>Morpholines (pharmacology)</term><term>Oncogene Protein v-akt (genetics)</term><term>Phosphorylation (MeSH)</term><term>Phosphotransferases (Alcohol Group Acceptor) (antagonists & inhibitors)</term><term>Phosphotransferases (Alcohol Group Acceptor) (genetics)</term><term>Receptors, Lysosphingolipid (antagonists & inhibitors)</term><term>Receptors, Lysosphingolipid (genetics)</term><term>Signal Transduction (drug effects)</term><term>Sphingosine (analogs & derivatives)</term><term>Sphingosine (biosynthesis)</term><term>Sphingosine (genetics)</term><term>Sphingosine N-Acyltransferase (genetics)</term><term>Sphingosine-1-Phosphate Receptors (MeSH)</term><term>TOR Serine-Threonine Kinases (genetics)</term><term>Triazines (pharmacology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Cellules MCF-7 (MeSH)</term><term>Céramides (biosynthèse)</term><term>Céramides (génétique)</term><term>Femelle (MeSH)</term><term>Humains (MeSH)</term><term>Lysophospholipides (biosynthèse)</term><term>Lysophospholipides (génétique)</term><term>Morpholines (pharmacologie)</term><term>Phosphorylation (MeSH)</term><term>Phosphotransferases (Alcohol Group Acceptor) (antagonistes et inhibiteurs)</term><term>Phosphotransferases (Alcohol Group Acceptor) (génétique)</term><term>Prolifération cellulaire (génétique)</term><term>Protéine oncogène v-akt (génétique)</term><term>Protéines membranaires (génétique)</term><term>Récepteurs aux lysosphingolipides (antagonistes et inhibiteurs)</term><term>Récepteurs aux lysosphingolipides (génétique)</term><term>Régulation de l'expression des gènes tumoraux (MeSH)</term><term>Sphingosine (analogues et dérivés)</term><term>Sphingosine (biosynthèse)</term><term>Sphingosine (génétique)</term><term>Sphingosine N-acyltransferase (génétique)</term><term>Système de signalisation des MAP kinases (effets des médicaments et des substances chimiques)</term><term>Sérine-thréonine kinases TOR (génétique)</term><term>Transduction du signal (effets des médicaments et des substances chimiques)</term><term>Triazines (pharmacologie)</term><term>Tumeurs du sein (anatomopathologie)</term><term>Tumeurs du sein (génétique)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Sphingosine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Phosphotransferases (Alcohol Group Acceptor)</term><term>Receptors, Lysosphingolipid</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Ceramides</term><term>Lysophospholipids</term><term>Sphingosine</term></keywords><keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>Sphingosine</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Tumeurs du sein</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Phosphotransferases (Alcohol Group Acceptor)</term><term>Récepteurs aux lysosphingolipides</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Céramides</term><term>Lysophospholipides</term><term>Sphingosine</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>MAP Kinase Signaling System</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Système de signalisation des MAP kinases</term><term>Transduction du signal</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Breast Neoplasms</term><term>Cell Proliferation</term><term>Ceramides</term><term>Lysophospholipids</term><term>Membrane Proteins</term><term>Oncogene Protein v-akt</term><term>Phosphotransferases (Alcohol Group Acceptor)</term><term>Receptors, Lysosphingolipid</term><term>Sphingosine</term><term>Sphingosine N-Acyltransferase</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Céramides</term><term>Lysophospholipides</term><term>Phosphotransferases (Alcohol Group Acceptor)</term><term>Prolifération cellulaire</term><term>Protéine oncogène v-akt</term><term>Protéines membranaires</term><term>Récepteurs aux lysosphingolipides</term><term>Sphingosine</term><term>Sphingosine N-acyltransferase</term><term>Sérine-thréonine kinases TOR</term><term>Tumeurs du sein</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Breast Neoplasms</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Morpholines</term><term>Triazines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Morpholines</term><term>Triazines</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Female</term><term>Gene Expression Regulation, Neoplastic</term><term>Humans</term><term>MCF-7 Cells</term><term>Phosphorylation</term><term>Sphingosine-1-Phosphate Receptors</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Cellules MCF-7</term><term>Femelle</term><term>Humains</term><term>Phosphorylation</term><term>Régulation de l'expression des gènes tumoraux</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Recently, sphingolipid derivatives, such as ceramide and sphingosine‑1‑phosphate (S1P), have emerged as key modulators in apoptotic cell death and cell proliferation. This study aimed to clarify the underlying signaling pathways of ceramide and S1P involved in breast cancer cell proliferation. Ceramide acyl chain length is determined by six mammalian ceramide synthases (CerS). We overexpressed CerS1 to 6 in MCF‑7 cells to examine whether ceramide signaling propagation varies as a function of acyl chain length. Among the six CerS, only CerS6 overexpression reduced phosphorylation of Akt, S6 kinase (S6K), and extracellular signal‑regulated kinases (ERK) as shown by western blotting. In addition, CerS6 overexpression reduced MCF‑7 cell proliferation. This effect was partially reversed by co‑treatment with MHY1485, an activator of mammalian target of rapamycin (mTOR), demonstrating an important role for the mTOR pathway in the CerS6‑mediated decrease in MCF‑7 cell proliferation. ERK inhibition, but not Akt inhibition, along with mTOR inhibition synergistically reduced MCF‑7 cell proliferation as measured by MTT assay. Notably, the expression of CerS6 and S1P receptor 2 (S1PR2), or CerS6 and sphingosine kinase 1 (SphK1), were negatively correlated according to the invasive breast carcinoma patient cohort in The Cancer Genome Atlas database. In addition, both SphK1 overexpression and S1P addition increased mTOR phosphorylation as shown by ELISA, while S1PR2 inhibition had the inverse effect. These data suggest that CerS6 and SphK1 regulate mTOR signaling in breast cancer cell proliferation. Moreover, mTOR activity can be regulated by the balance between S1P and C16‑ceramide, which is generated by CerS6.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30226616</PMID><DateCompleted><Year>2018</Year><Month>12</Month><Day>18</Day></DateCompleted><DateRevised><Year>2019</Year><Month>12</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1791-2431</ISSN><JournalIssue CitedMedium="Internet"><Volume>40</Volume><Issue>5</Issue><PubDate><Year>2018</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Oncology reports</Title><ISOAbbreviation>Oncol Rep</ISOAbbreviation></Journal><ArticleTitle>C16‑ceramide and sphingosine 1‑phosphate/S1PR2 have opposite effects on cell growth through mTOR signaling pathway regulation.</ArticleTitle><Pagination><MedlinePgn>2977-2987</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3892/or.2018.6689</ELocationID><Abstract><AbstractText>Recently, sphingolipid derivatives, such as ceramide and sphingosine‑1‑phosphate (S1P), have emerged as key modulators in apoptotic cell death and cell proliferation. This study aimed to clarify the underlying signaling pathways of ceramide and S1P involved in breast cancer cell proliferation. Ceramide acyl chain length is determined by six mammalian ceramide synthases (CerS). We overexpressed CerS1 to 6 in MCF‑7 cells to examine whether ceramide signaling propagation varies as a function of acyl chain length. Among the six CerS, only CerS6 overexpression reduced phosphorylation of Akt, S6 kinase (S6K), and extracellular signal‑regulated kinases (ERK) as shown by western blotting. In addition, CerS6 overexpression reduced MCF‑7 cell proliferation. This effect was partially reversed by co‑treatment with MHY1485, an activator of mammalian target of rapamycin (mTOR), demonstrating an important role for the mTOR pathway in the CerS6‑mediated decrease in MCF‑7 cell proliferation. ERK inhibition, but not Akt inhibition, along with mTOR inhibition synergistically reduced MCF‑7 cell proliferation as measured by MTT assay. Notably, the expression of CerS6 and S1P receptor 2 (S1PR2), or CerS6 and sphingosine kinase 1 (SphK1), were negatively correlated according to the invasive breast carcinoma patient cohort in The Cancer Genome Atlas database. In addition, both SphK1 overexpression and S1P addition increased mTOR phosphorylation as shown by ELISA, while S1PR2 inhibition had the inverse effect. These data suggest that CerS6 and SphK1 regulate mTOR signaling in breast cancer cell proliferation. Moreover, mTOR activity can be regulated by the balance between S1P and C16‑ceramide, which is generated by CerS6.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Min Hee</ForeName><Initials>MH</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, College of Medicine, Gachon University, Incheon 21999, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>Joo-Won</ForeName><Initials>JW</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, College of Medicine, Ewha Womans University, Seoul 07985, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Eun-Ji</ForeName><Initials>EJ</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, College of Medicine, Gachon University, Incheon 21999, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Shin</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Immunology, School of Medicine, Keimyung University, Daegu 42601, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shin</LastName><ForeName>Sun-Hye</ForeName><Initials>SH</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, College of Medicine, Ewha Womans University, Seoul 07985, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ahn</LastName><ForeName>Jung-Hyuck</ForeName><Initials>JH</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, College of Medicine, Ewha Womans University, Seoul 07985, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jung</LastName><ForeName>Yunjae</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Microbiology, College of Medicine, Gachon University, Incheon 21999, Division of Medical Oncology, Department of Internal Medicine, Gachon University Gil Medical Center, Incheon 21565, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>Inkeun</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Division of Medical Oncology, Department of Internal Medicine, Gachon University Gil Medical Center, Incheon 21565, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>Woo-Jae</ForeName><Initials>WJ</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, College of Medicine, Gachon University, Incheon 21999, Republic of Korea.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2018</Year><Month>09</Month><Day>07</Day></ArticleDate></Article><MedlineJournalInfo><Country>Greece</Country><MedlineTA>Oncol Rep</MedlineTA><NlmUniqueID>9422756</NlmUniqueID><ISSNLinking>1021-335X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C577756">4,6-dimorpholino-N-(4-nitrophenyl)-1,3,5-triazin-2-amine</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002518">Ceramides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008246">Lysophospholipids</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008565">Membrane Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009025">Morpholines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D049349">Receptors, Lysosphingolipid</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C477522">S1PR2 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000081025">Sphingosine-1-Phosphate Receptors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014227">Triazines</NameOfSubstance></Chemical><Chemical><RegistryNumber>26993-30-6</RegistryNumber><NameOfSubstance UI="C060506">sphingosine 1-phosphate</NameOfSubstance></Chemical><Chemical><RegistryNumber>4201-58-5</RegistryNumber><NameOfSubstance UI="C097760">N-palmitoylsphingosine</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.3.1.24</RegistryNumber><NameOfSubstance UI="C493790">CERS1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.3.1.24</RegistryNumber><NameOfSubstance UI="C506123">CERS6 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.3.1.24</RegistryNumber><NameOfSubstance UI="D051049">Sphingosine N-Acyltransferase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.-</RegistryNumber><NameOfSubstance UI="D017853">Phosphotransferases (Alcohol Group Acceptor)</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.-</RegistryNumber><NameOfSubstance UI="C022648">sphingosine kinase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="C546842">MTOR protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D051058">Oncogene Protein v-akt</NameOfSubstance></Chemical><Chemical><RegistryNumber>NGZ37HRE42</RegistryNumber><NameOfSubstance UI="D013110">Sphingosine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001943" MajorTopicYN="N">Breast Neoplasms</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002518" MajorTopicYN="N">Ceramides</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015972" MajorTopicYN="N">Gene Expression Regulation, Neoplastic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008246" MajorTopicYN="N">Lysophospholipids</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020935" MajorTopicYN="N">MAP Kinase Signaling System</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D061986" MajorTopicYN="N">MCF-7 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008565" MajorTopicYN="N">Membrane Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009025" MajorTopicYN="N">Morpholines</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051058" MajorTopicYN="N">Oncogene Protein v-akt</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010766" MajorTopicYN="N">Phosphorylation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017853" MajorTopicYN="N">Phosphotransferases (Alcohol Group Acceptor)</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049349" MajorTopicYN="N">Receptors, Lysosphingolipid</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013110" MajorTopicYN="N">Sphingosine</DescriptorName><QualifierName UI="Q000031" MajorTopicYN="N">analogs & derivatives</QualifierName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051049" MajorTopicYN="N">Sphingosine N-Acyltransferase</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000081025" MajorTopicYN="N">Sphingosine-1-Phosphate Receptors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014227" MajorTopicYN="N">Triazines</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year><Month>03</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2018</Year><Month>07</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2018</Year><Month>9</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2018</Year><Month>12</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2018</Year><Month>9</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30226616</ArticleId><ArticleId IdType="doi">10.3892/or.2018.6689</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Corée du Sud</li></country><region><li>Région capitale de Séoul</li></region><settlement><li>Séoul</li></settlement></list><tree><country name="Corée du Sud"><noRegion><name sortKey="Kim, Min Hee" sort="Kim, Min Hee" uniqKey="Kim M" first="Min Hee" last="Kim">Min Hee Kim</name></noRegion><name sortKey="Ahn, Jung Hyuck" sort="Ahn, Jung Hyuck" uniqKey="Ahn J" first="Jung-Hyuck" last="Ahn">Jung-Hyuck Ahn</name><name sortKey="Jung, Yunjae" sort="Jung, Yunjae" uniqKey="Jung Y" first="Yunjae" last="Jung">Yunjae Jung</name><name sortKey="Kim, Shin" sort="Kim, Shin" uniqKey="Kim S" first="Shin" last="Kim">Shin Kim</name><name sortKey="Lee, Eun Ji" sort="Lee, Eun Ji" uniqKey="Lee E" first="Eun-Ji" last="Lee">Eun-Ji Lee</name><name sortKey="Park, Inkeun" sort="Park, Inkeun" uniqKey="Park I" first="Inkeun" last="Park">Inkeun Park</name><name sortKey="Park, Joo Won" sort="Park, Joo Won" uniqKey="Park J" first="Joo-Won" last="Park">Joo-Won Park</name><name sortKey="Park, Woo Jae" sort="Park, Woo Jae" uniqKey="Park W" first="Woo-Jae" last="Park">Woo-Jae Park</name><name sortKey="Shin, Sun Hye" sort="Shin, Sun Hye" uniqKey="Shin S" first="Sun-Hye" last="Shin">Sun-Hye Shin</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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