RapamycinFungusV1, Main, Exploration, bibRecord, 000530

PFK15, a PFKFB3 antagonist, inhibits autophagy and proliferation in rhabdomyosarcoma cells.

Identifieur interne : 000530 ( Main/Exploration ); précédent : 000529; suivant : 000531

PFK15, a PFKFB3 antagonist, inhibits autophagy and proliferation in rhabdomyosarcoma cells.

Auteurs : Chunhui Wang [République populaire de Chine] ; Jianghong Qu [République populaire de Chine] ; Siyuan Yan [République populaire de Chine] ; Quan Gao [République populaire de Chine] ; Sibin Hao [République populaire de Chine] ; Dongsheng Zhou [République populaire de Chine]

Source :

International journal of molecular medicine [ 1791-244X ] ; 2018.

RBID : pubmed:29620138

Descripteurs français

KwdFr :
- 5-Amino-imidazole-4-carboxamide (analogues et dérivés), 5-Amino-imidazole-4-carboxamide (pharmacologie), Adenylate kinase (métabolisme), Autophagie (effets des médicaments et des substances chimiques), Clones cellulaires (MeSH), Complexe-1 cible mécanistique de la rapamycine (métabolisme), Humains (MeSH), Inhibiteurs de protéines kinases (pharmacologie), Lignée cellulaire tumorale (MeSH), Noyau de la cellule (anatomopathologie), Noyau de la cellule (effets des médicaments et des substances chimiques), Phosphofructokinase-2 (antagonistes et inhibiteurs), Phosphofructokinase-2 (métabolisme), Phosphorylation (effets des médicaments et des substances chimiques), Poly(ADP-ribose) polymerases (métabolisme), Prolifération cellulaire (effets des médicaments et des substances chimiques), Protéines proto-oncogènes c-akt (métabolisme), Pyridines (pharmacologie), Quinoléines (pharmacologie), Rhabdomyosarcome (anatomopathologie), Rhabdomyosarcome (ultrastructure), Ribonucléotides (pharmacologie), Régulation négative (effets des médicaments et des substances chimiques), Survie cellulaire (effets des médicaments et des substances chimiques).
MESH :
- analogues et dérivés : 5-Amino-imidazole-4-carboxamide.
- anatomopathologie : Noyau de la cellule, Rhabdomyosarcome.
- antagonistes et inhibiteurs : Phosphofructokinase-2.
- effets des médicaments et des substances chimiques : Autophagie, Noyau de la cellule, Phosphorylation, Prolifération cellulaire, Régulation négative, Survie cellulaire.
- métabolisme : Adenylate kinase, Complexe-1 cible mécanistique de la rapamycine, Phosphofructokinase-2, Poly(ADP-ribose) polymerases, Protéines proto-oncogènes c-akt.
- pharmacologie : 5-Amino-imidazole-4-carboxamide, Inhibiteurs de protéines kinases, Pyridines, Quinoléines, Ribonucléotides.
- ultrastructure : Clones cellulaires, Humains, Lignée cellulaire tumorale, Rhabdomyosarcome.

English descriptors

KwdEn :
- Adenylate Kinase (metabolism), Aminoimidazole Carboxamide (analogs & derivatives), Aminoimidazole Carboxamide (pharmacology), Autophagy (drug effects), Cell Line, Tumor (MeSH), Cell Nucleus (drug effects), Cell Nucleus (pathology), Cell Proliferation (drug effects), Cell Survival (drug effects), Clone Cells (MeSH), Down-Regulation (drug effects), Humans (MeSH), Mechanistic Target of Rapamycin Complex 1 (metabolism), Phosphofructokinase-2 (antagonists & inhibitors), Phosphofructokinase-2 (metabolism), Phosphorylation (drug effects), Poly(ADP-ribose) Polymerases (metabolism), Protein Kinase Inhibitors (pharmacology), Proto-Oncogene Proteins c-akt (metabolism), Pyridines (pharmacology), Quinolines (pharmacology), Rhabdomyosarcoma (pathology), Rhabdomyosarcoma (ultrastructure), Ribonucleotides (pharmacology).
MESH :
- chemical , analogs & derivatives : Aminoimidazole Carboxamide.
- chemical , antagonists & inhibitors : Phosphofructokinase-2.
- chemical , metabolism : Adenylate Kinase, Mechanistic Target of Rapamycin Complex 1, Phosphofructokinase-2, Poly(ADP-ribose) Polymerases, Proto-Oncogene Proteins c-akt.
- chemical , pharmacology : Aminoimidazole Carboxamide, Protein Kinase Inhibitors, Pyridines, Quinolines, Ribonucleotides.
- drug effects : Autophagy, Cell Nucleus, Cell Proliferation, Cell Survival, Down-Regulation, Phosphorylation.
- pathology : Cell Nucleus, Rhabdomyosarcoma.
- ultrastructure : Rhabdomyosarcoma.
- Cell Line, Tumor, Clone Cells, Humans.

Abstract

Due to the high-level of metastatic and relapsed rates, rhabdomyosarcoma (RD) patients have a poor prognosis, and novel treatment strategies are required. Thereby, the present study evaluated the efficacy of PFK15, a PFKFB3 inhibitor, in RD cells to explore its potential underlying mechanism on the regulation of autophagy and proliferation in these cells. The effects of PFK15 on cell viability loss and cell death in different treatment groups, were evaluated by MTS assay, colony growth assay and immunoblotting, respectively. In addition, the autophagy levels were detected by electron microscopy, fluorescence microscopy and immunoblotting following PFK15 treatment, and the autophagic flux was analyzed with the addition of chloroquine diphosphate salt or by monitoring the level of p62. PFK15 was observed to evidently decrease the viability of RD cells, inhibit the colony growth and cause abnormal nuclear morphology. Furthermore, PFK15 inhibited the autophagic flux and cell proliferation, as well as induced apoptotic cell death in RD cells through downregulation of the adenosine monophosphate‑activated protein kinase (AMPK) signaling pathway. An AMPK agonist rescued the inhibited cell proliferation and autophagy induced by PFK15. In conclusion, PFK15 inhibits autophagy and cell proliferation via downregulating the AMPK signaling pathway in RD cells.

DOI: 10.3892/ijmm.2018.3599
PubMed: 29620138
PubMed Central: PMC5979828

Affiliations:

Links toward previous steps (curation, corpus...)

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Le document en format XML

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<affiliation wicri:level="1"><nlm:affiliation>Department of Orthopedics, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, P.R. China.</nlm:affiliation>
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<author><name sortKey="Zhou, Dongsheng" sort="Zhou, Dongsheng" uniqKey="Zhou D" first="Dongsheng" last="Zhou">Dongsheng Zhou</name>
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<term>Aminoimidazole Carboxamide (analogs & derivatives)</term>
<term>Aminoimidazole Carboxamide (pharmacology)</term>
<term>Autophagy (drug effects)</term>
<term>Cell Line, Tumor (MeSH)</term>
<term>Cell Nucleus (drug effects)</term>
<term>Cell Nucleus (pathology)</term>
<term>Cell Proliferation (drug effects)</term>
<term>Cell Survival (drug effects)</term>
<term>Clone Cells (MeSH)</term>
<term>Down-Regulation (drug effects)</term>
<term>Humans (MeSH)</term>
<term>Mechanistic Target of Rapamycin Complex 1 (metabolism)</term>
<term>Phosphofructokinase-2 (antagonists & inhibitors)</term>
<term>Phosphofructokinase-2 (metabolism)</term>
<term>Phosphorylation (drug effects)</term>
<term>Poly(ADP-ribose) Polymerases (metabolism)</term>
<term>Protein Kinase Inhibitors (pharmacology)</term>
<term>Proto-Oncogene Proteins c-akt (metabolism)</term>
<term>Pyridines (pharmacology)</term>
<term>Quinolines (pharmacology)</term>
<term>Rhabdomyosarcoma (pathology)</term>
<term>Rhabdomyosarcoma (ultrastructure)</term>
<term>Ribonucleotides (pharmacology)</term>
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<term>5-Amino-imidazole-4-carboxamide (pharmacologie)</term>
<term>Adenylate kinase (métabolisme)</term>
<term>Autophagie (effets des médicaments et des substances chimiques)</term>
<term>Clones cellulaires (MeSH)</term>
<term>Complexe-1 cible mécanistique de la rapamycine (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Inhibiteurs de protéines kinases (pharmacologie)</term>
<term>Lignée cellulaire tumorale (MeSH)</term>
<term>Noyau de la cellule (anatomopathologie)</term>
<term>Noyau de la cellule (effets des médicaments et des substances chimiques)</term>
<term>Phosphofructokinase-2 (antagonistes et inhibiteurs)</term>
<term>Phosphofructokinase-2 (métabolisme)</term>
<term>Phosphorylation (effets des médicaments et des substances chimiques)</term>
<term>Poly(ADP-ribose) polymerases (métabolisme)</term>
<term>Prolifération cellulaire (effets des médicaments et des substances chimiques)</term>
<term>Protéines proto-oncogènes c-akt (métabolisme)</term>
<term>Pyridines (pharmacologie)</term>
<term>Quinoléines (pharmacologie)</term>
<term>Rhabdomyosarcome (anatomopathologie)</term>
<term>Rhabdomyosarcome (ultrastructure)</term>
<term>Ribonucléotides (pharmacologie)</term>
<term>Régulation négative (effets des médicaments et des substances chimiques)</term>
<term>Survie cellulaire (effets des médicaments et des substances chimiques)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Aminoimidazole Carboxamide</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Phosphofructokinase-2</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adenylate Kinase</term>
<term>Mechanistic Target of Rapamycin Complex 1</term>
<term>Phosphofructokinase-2</term>
<term>Poly(ADP-ribose) Polymerases</term>
<term>Proto-Oncogene Proteins c-akt</term>
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<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Aminoimidazole Carboxamide</term>
<term>Protein Kinase Inhibitors</term>
<term>Pyridines</term>
<term>Quinolines</term>
<term>Ribonucleotides</term>
</keywords>
<keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>5-Amino-imidazole-4-carboxamide</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Noyau de la cellule</term>
<term>Rhabdomyosarcome</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Phosphofructokinase-2</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term>
<term>Cell Nucleus</term>
<term>Cell Proliferation</term>
<term>Cell Survival</term>
<term>Down-Regulation</term>
<term>Phosphorylation</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Autophagie</term>
<term>Noyau de la cellule</term>
<term>Phosphorylation</term>
<term>Prolifération cellulaire</term>
<term>Régulation négative</term>
<term>Survie cellulaire</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Adenylate kinase</term>
<term>Complexe-1 cible mécanistique de la rapamycine</term>
<term>Phosphofructokinase-2</term>
<term>Poly(ADP-ribose) polymerases</term>
<term>Protéines proto-oncogènes c-akt</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Cell Nucleus</term>
<term>Rhabdomyosarcoma</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>5-Amino-imidazole-4-carboxamide</term>
<term>Inhibiteurs de protéines kinases</term>
<term>Pyridines</term>
<term>Quinoléines</term>
<term>Ribonucléotides</term>
</keywords>
<keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Rhabdomyosarcoma</term>
</keywords>
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<term>Clone Cells</term>
<term>Humans</term>
</keywords>
<keywords scheme="MESH" qualifier="ultrastructure" xml:lang="fr"><term>Clones cellulaires</term>
<term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Rhabdomyosarcome</term>
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<front><div type="abstract" xml:lang="en">Due to the high-level of metastatic and relapsed rates, rhabdomyosarcoma (RD) patients have a poor prognosis, and novel treatment strategies are required. Thereby, the present study evaluated the efficacy of PFK15, a PFKFB3 inhibitor, in RD cells to explore its potential underlying mechanism on the regulation of autophagy and proliferation in these cells. The effects of PFK15 on cell viability loss and cell death in different treatment groups, were evaluated by MTS assay, colony growth assay and immunoblotting, respectively. In addition, the autophagy levels were detected by electron microscopy, fluorescence microscopy and immunoblotting following PFK15 treatment, and the autophagic flux was analyzed with the addition of chloroquine diphosphate salt or by monitoring the level of p62. PFK15 was observed to evidently decrease the viability of RD cells, inhibit the colony growth and cause abnormal nuclear morphology. Furthermore, PFK15 inhibited the autophagic flux and cell proliferation, as well as induced apoptotic cell death in RD cells through downregulation of the adenosine monophosphate‑activated protein kinase (AMPK) signaling pathway. An AMPK agonist rescued the inhibited cell proliferation and autophagy induced by PFK15. In conclusion, PFK15 inhibits autophagy and cell proliferation via downregulating the AMPK signaling pathway in RD cells.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29620138</PMID>
<DateCompleted><Year>2018</Year>
<Month>09</Month>
<Day>24</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>14</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1791-244X</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>42</Volume>
<Issue>1</Issue>
<PubDate><Year>2018</Year>
<Month>Jul</Month>
</PubDate>
</JournalIssue>
<Title>International journal of molecular medicine</Title>
<ISOAbbreviation>Int J Mol Med</ISOAbbreviation>
</Journal>
<ArticleTitle>PFK15, a PFKFB3 antagonist, inhibits autophagy and proliferation in rhabdomyosarcoma cells.</ArticleTitle>
<Pagination><MedlinePgn>359-367</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.3892/ijmm.2018.3599</ELocationID>
<Abstract><AbstractText>Due to the high-level of metastatic and relapsed rates, rhabdomyosarcoma (RD) patients have a poor prognosis, and novel treatment strategies are required. Thereby, the present study evaluated the efficacy of PFK15, a PFKFB3 inhibitor, in RD cells to explore its potential underlying mechanism on the regulation of autophagy and proliferation in these cells. The effects of PFK15 on cell viability loss and cell death in different treatment groups, were evaluated by MTS assay, colony growth assay and immunoblotting, respectively. In addition, the autophagy levels were detected by electron microscopy, fluorescence microscopy and immunoblotting following PFK15 treatment, and the autophagic flux was analyzed with the addition of chloroquine diphosphate salt or by monitoring the level of p62. PFK15 was observed to evidently decrease the viability of RD cells, inhibit the colony growth and cause abnormal nuclear morphology. Furthermore, PFK15 inhibited the autophagic flux and cell proliferation, as well as induced apoptotic cell death in RD cells through downregulation of the adenosine monophosphate‑activated protein kinase (AMPK) signaling pathway. An AMPK agonist rescued the inhibited cell proliferation and autophagy induced by PFK15. In conclusion, PFK15 inhibits autophagy and cell proliferation via downregulating the AMPK signaling pathway in RD cells.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Chunhui</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Department of Orthopedics, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, P.R. China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Qu</LastName>
<ForeName>Jianghong</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Gynecology, Zhangqiu People's Hospital, Jinan, Shandong 250200, P.R. China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yan</LastName>
<ForeName>Siyuan</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Mycology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, P.R. China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Gao</LastName>
<ForeName>Quan</ForeName>
<Initials>Q</Initials>
<AffiliationInfo><Affiliation>State Key Laboratory of Mycology, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, P.R. China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hao</LastName>
<ForeName>Sibin</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Orthopedics, Zhangqiu People's Hospital, Jinan, Shandong 250200, P.R. China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhou</LastName>
<ForeName>Dongsheng</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Department of Orthopedics, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, P.R. China.</Affiliation>
</AffiliationInfo>
</Author>
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<ReferenceList><Reference><Citation>Biochem J. 1980 Dec 15;192(3):897-901</Citation>
<ArticleIdList><ArticleId IdType="pubmed">6453589</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2006 Nov 28;103(48):18308-13</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17116882</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 2008 Feb 15;283(7):3979-87</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18056705</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Biochem Biophys Res Commun. 2017 Feb 5;483(2):897-903</Citation>
<ArticleIdList><ArticleId IdType="pubmed">28082200</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>BMC Cancer. 2009 Sep 01;9:307</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19723334</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Exp Mol Pathol. 2009 Jun;86(3):174-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19454274</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Autophagy. 2009 Jan;5(1):61-74</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19001878</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Biochem Biophys Res Commun. 2015 Aug 28;464(3):862-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">26171876</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cancer Lett. 2015 Jan 28;356(2 Pt A):165-70</Citation>
<ArticleIdList><ArticleId IdType="pubmed">24486219</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell. 2011 Nov 11;147(4):728-41</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22078875</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cancer Res. 2015 Jul;13(7):1059-72</Citation>
<ArticleIdList><ArticleId IdType="pubmed">25956158</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Biochem J. 2012 Mar 1;442(2):345-56</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22115192</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>FEBS Lett. 2006 May 29;580(13):3308-14</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16698023</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Surg Oncol. 2007 Nov;16(3):173-85</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17689957</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Autophagy. 2013 Sep;9(9):1443-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23881027</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Biochim Biophys Acta. 2011 Jun;1807(6):707-18</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21692240</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Clin Cancer Res. 2005 Aug 15;11(16):5784-92</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16115917</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell. 2011 Mar 4;144(5):646-74</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21376230</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Clin Cancer Res. 2015 Nov 15;21(22):5037-46</Citation>
<ArticleIdList><ArticleId IdType="pubmed">26567363</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Oncol Rep. 2016 Aug;36(2):945-51</Citation>
<ArticleIdList><ArticleId IdType="pubmed">27373212</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Bioessays. 2004 Aug;26(8):882-93</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15273990</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Transl Med. 2012 May 16;10:95</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22591674</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Breast Cancer Res Treat. 2016 Nov;160(1):29-40</Citation>
<ArticleIdList><ArticleId IdType="pubmed">27613609</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Autophagy. 2016;12 (1):1-222</Citation>
<ArticleIdList><ArticleId IdType="pubmed">26799652</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cancer Biol Ther. 2002 Mar-Apr;1(2):97-104</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12170781</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cancer Res. 1993 Sep 1;53(17):3976-85</Citation>
<ArticleIdList><ArticleId IdType="pubmed">8358726</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Anticancer Res. 2016 Apr;36(4):1479-88</Citation>
<ArticleIdList><ArticleId IdType="pubmed">27069123</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 1981 Jun;78(6):3483-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">6455662</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cancer Metab. 2013 Feb 04;1(1):8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">24280138</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cancer Ther. 2013 Aug;12(8):1461-70</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23674815</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Pediatr Blood Cancer. 2012 Jul 15;59(1):5-10</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22378628</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>PLoS One. 2013;8(2):e56966</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23437282</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cancer Res. 2002 Oct 15;62(20):5881-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12384552</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Med Oncol. 2011 Mar;28(1):105-11</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20041317</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>FEBS J. 2013 Sep;280(17):4323-34</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23822136</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Exp Clin Cancer Res. 2017 Jan 7;36(1):7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">28061878</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cancer Res. 2007 Jul 15;67(14):6745-52</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17638885</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Ann Transl Med. 2014 Jun;2(6):57</Citation>
<ArticleIdList><ArticleId IdType="pubmed">25333032</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>PLoS One. 2016 Sep 26;11(9):e0163768</Citation>
<ArticleIdList><ArticleId IdType="pubmed">27669567</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Curr Oncol Rep. 2010 Nov;12(6):402-10</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20820958</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Biochem J. 1999 Sep 1;342 ( Pt 2):249-68</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10455009</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Trends Biochem Sci. 2004 Jan;29(1):18-24</Citation>
<ArticleIdList><ArticleId IdType="pubmed">14729328</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Korean J Intern Med. 2016 Mar;31(2):375-85</Citation>
<ArticleIdList><ArticleId IdType="pubmed">26701229</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Future Oncol. 2010 Mar;6(3):457-70</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20222801</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cancer Res. 2009 Feb 1;69(3):923-31</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19176390</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cancer Lett. 1990 Apr 30;50(3):173-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">2157546</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
</PubmedData>
</pubmed>
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<name sortKey="Yan, Siyuan" sort="Yan, Siyuan" uniqKey="Yan S" first="Siyuan" last="Yan">Siyuan Yan</name>
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	Serveur d'exploration sur la rapamycine et les champignons
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Serveur d'exploration sur la rapamycine et les champignons

PFK15, a PFKFB3 antagonist, inhibits autophagy and proliferation in rhabdomyosarcoma cells.

PFK15, a PFKFB3 antagonist, inhibits autophagy and proliferation in rhabdomyosarcoma cells.

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