RapamycinFungusV1, Main, Exploration, bibRecord, 000A47

Perfluorooctanoic acid induces human Ishikawa endometrial cancer cell migration and invasion through activation of ERK/mTOR signaling.

Identifieur interne : 000A47 ( Main/Exploration ); précédent : 000A46; suivant : 000A48

Perfluorooctanoic acid induces human Ishikawa endometrial cancer cell migration and invasion through activation of ERK/mTOR signaling.

Auteurs : Zhinan Ma [République populaire de Chine] ; Xiaoqiu Liu [République populaire de Chine] ; Fujun Li [République populaire de Chine] ; Yixong Wang [République populaire de Chine] ; Yang Xu [République populaire de Chine] ; Mei Zhang [République populaire de Chine] ; Xiaoqian Zhang [République populaire de Chine] ; Xiaoyan Ying [République populaire de Chine] ; Xuesen Zhang [République populaire de Chine]

Source :

Oncotarget [ 1949-2553 ] ; 2016.

RBID : pubmed:27589685

Descripteurs français

English descriptors

KwdEn :
- Animals (MeSH), Caprylates (toxicity), Carcinogens (toxicity), Cell Line, Tumor (MeSH), Cell Movement (drug effects), Endometrial Neoplasms (metabolism), Endometrial Neoplasms (pathology), Enzyme Activation (drug effects), Epithelial-Mesenchymal Transition (drug effects), Female (MeSH), Fluorocarbons (toxicity), Heterografts (MeSH), Humans (MeSH), MAP Kinase Signaling System (drug effects), Mice (MeSH), Mice, Inbred BALB C (MeSH), Mice, Nude (MeSH), Neoplasm Invasiveness (pathology), Signal Transduction (drug effects), TOR Serine-Threonine Kinases (drug effects), TOR Serine-Threonine Kinases (metabolism).
MESH :
- chemical , drug effects : TOR Serine-Threonine Kinases.
- chemical , metabolism : TOR Serine-Threonine Kinases.
- chemical , toxicity : Caprylates, Carcinogens, Fluorocarbons.
- drug effects : Cell Movement, Enzyme Activation, Epithelial-Mesenchymal Transition, MAP Kinase Signaling System, Signal Transduction.
- metabolism : Endometrial Neoplasms.
- pathology : Endometrial Neoplasms, Neoplasm Invasiveness.
- Animals, Cell Line, Tumor, Female, Heterografts, Humans, Mice, Mice, Inbred BALB C, Mice, Nude.

Abstract

Perfluorooctanoic acid (PFOA) is a common environmental pollutant that has been associated with various diseases, including cancer. We explored the molecular mechanisms underlying PFOA-induced endometrial cancer cell invasion and migration. PFOA treatment enhanced migration and invasion by human Ishikawa endometrial cancer cells, which correlated with decreased E-cadherin expression, a marker of epithelial-mesenchymal transition. PFOA also induced activation of ERK1/2/mTOR signaling. Treatment with rapamycin, an mTOR inhibitor, antagonized the effects of PFOA and reversed the effects of PFOA activation in a xenograft mouse model of endometrial cancer. Consistent with these results, pre-treatment with rapamycin abolished PFOA-induced down-regulation of E-cadherin expression. These results indicate that PFOA is a carcinogen that promotes endometrial cancer cell migration and invasion through activation of ERK/mTOR signaling.

DOI: 10.18632/oncotarget.11684
PubMed: 27589685
PubMed Central: PMC5341820

Affiliations:

République populaire de Chine

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

to stream Main, to step Corpus: 000976
to stream Main, to step Curation: 000976

Le document en format XML

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<term>Caprylates (toxicity)</term>
<term>Carcinogens (toxicity)</term>
<term>Cell Line, Tumor (MeSH)</term>
<term>Cell Movement (drug effects)</term>
<term>Endometrial Neoplasms (metabolism)</term>
<term>Endometrial Neoplasms (pathology)</term>
<term>Enzyme Activation (drug effects)</term>
<term>Epithelial-Mesenchymal Transition (drug effects)</term>
<term>Female (MeSH)</term>
<term>Fluorocarbons (toxicity)</term>
<term>Heterografts (MeSH)</term>
<term>Humans (MeSH)</term>
<term>MAP Kinase Signaling System (drug effects)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred BALB C (MeSH)</term>
<term>Mice, Nude (MeSH)</term>
<term>Neoplasm Invasiveness (pathology)</term>
<term>Signal Transduction (drug effects)</term>
<term>TOR Serine-Threonine Kinases (drug effects)</term>
<term>TOR Serine-Threonine Kinases (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Activation enzymatique (effets des médicaments et des substances chimiques)</term>
<term>Animaux (MeSH)</term>
<term>Cancérogènes (toxicité)</term>
<term>Caprylates (toxicité)</term>
<term>Femelle (MeSH)</term>
<term>Fluorocarbones (toxicité)</term>
<term>Humains (MeSH)</term>
<term>Hétérogreffes (MeSH)</term>
<term>Invasion tumorale (anatomopathologie)</term>
<term>Lignée cellulaire tumorale (MeSH)</term>
<term>Mouvement cellulaire (effets des médicaments et des substances chimiques)</term>
<term>Souris (MeSH)</term>
<term>Souris de lignée BALB C (MeSH)</term>
<term>Souris nude (MeSH)</term>
<term>Système de signalisation des MAP kinases (effets des médicaments et des substances chimiques)</term>
<term>Sérine-thréonine kinases TOR (effets des médicaments et des substances chimiques)</term>
<term>Sérine-thréonine kinases TOR (métabolisme)</term>
<term>Transduction du signal (effets des médicaments et des substances chimiques)</term>
<term>Transition épithélio-mésenchymateuse (effets des médicaments et des substances chimiques)</term>
<term>Tumeurs de l'endomètre (anatomopathologie)</term>
<term>Tumeurs de l'endomètre (métabolisme)</term>
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</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>TOR Serine-Threonine Kinases</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Caprylates</term>
<term>Carcinogens</term>
<term>Fluorocarbons</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Invasion tumorale</term>
<term>Tumeurs de l'endomètre</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Movement</term>
<term>Enzyme Activation</term>
<term>Epithelial-Mesenchymal Transition</term>
<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>Activation enzymatique</term>
<term>Mouvement cellulaire</term>
<term>Système de signalisation des MAP kinases</term>
<term>Sérine-thréonine kinases TOR</term>
<term>Transduction du signal</term>
<term>Transition épithélio-mésenchymateuse</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Endometrial Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Sérine-thréonine kinases TOR</term>
<term>Tumeurs de l'endomètre</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Endometrial Neoplasms</term>
<term>Neoplasm Invasiveness</term>
</keywords>
<keywords scheme="MESH" qualifier="toxicité" xml:lang="fr"><term>Cancérogènes</term>
<term>Caprylates</term>
<term>Fluorocarbones</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Line, Tumor</term>
<term>Female</term>
<term>Heterografts</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Mice, Nude</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Femelle</term>
<term>Humains</term>
<term>Hétérogreffes</term>
<term>Lignée cellulaire tumorale</term>
<term>Souris</term>
<term>Souris de lignée BALB C</term>
<term>Souris nude</term>
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<front><div type="abstract" xml:lang="en">Perfluorooctanoic acid (PFOA) is a common environmental pollutant that has been associated with various diseases, including cancer. We explored the molecular mechanisms underlying PFOA-induced endometrial cancer cell invasion and migration. PFOA treatment enhanced migration and invasion by human Ishikawa endometrial cancer cells, which correlated with decreased E-cadherin expression, a marker of epithelial-mesenchymal transition. PFOA also induced activation of ERK1/2/mTOR signaling. Treatment with rapamycin, an mTOR inhibitor, antagonized the effects of PFOA and reversed the effects of PFOA activation in a xenograft mouse model of endometrial cancer. Consistent with these results, pre-treatment with rapamycin abolished PFOA-induced down-regulation of E-cadherin expression. These results indicate that PFOA is a carcinogen that promotes endometrial cancer cell migration and invasion through activation of ERK/mTOR signaling.</div>
</front>
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<DateCompleted><Year>2018</Year>
<Month>02</Month>
<Day>09</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1949-2553</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>7</Volume>
<Issue>41</Issue>
<PubDate><Year>2016</Year>
<Month>Oct</Month>
<Day>11</Day>
</PubDate>
</JournalIssue>
<Title>Oncotarget</Title>
<ISOAbbreviation>Oncotarget</ISOAbbreviation>
</Journal>
<ArticleTitle>Perfluorooctanoic acid induces human Ishikawa endometrial cancer cell migration and invasion through activation of ERK/mTOR signaling.</ArticleTitle>
<Pagination><MedlinePgn>66558-66568</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.18632/oncotarget.11684</ELocationID>
<Abstract><AbstractText>Perfluorooctanoic acid (PFOA) is a common environmental pollutant that has been associated with various diseases, including cancer. We explored the molecular mechanisms underlying PFOA-induced endometrial cancer cell invasion and migration. PFOA treatment enhanced migration and invasion by human Ishikawa endometrial cancer cells, which correlated with decreased E-cadherin expression, a marker of epithelial-mesenchymal transition. PFOA also induced activation of ERK1/2/mTOR signaling. Treatment with rapamycin, an mTOR inhibitor, antagonized the effects of PFOA and reversed the effects of PFOA activation in a xenograft mouse model of endometrial cancer. Consistent with these results, pre-treatment with rapamycin abolished PFOA-induced down-regulation of E-cadherin expression. These results indicate that PFOA is a carcinogen that promotes endometrial cancer cell migration and invasion through activation of ERK/mTOR signaling.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ma</LastName>
<ForeName>Zhinan</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Obstetrics and Gynecology, Yangzhou Maternal and Child Health Hospital, Yangzhou University, Yangzhou, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Liu</LastName>
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   |texte=   Perfluorooctanoic acid induces human Ishikawa endometrial cancer cell migration and invasion through activation of ERK/mTOR signaling.
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Perfluorooctanoic acid induces human Ishikawa endometrial cancer cell migration and invasion through activation of ERK/mTOR signaling.

Perfluorooctanoic acid induces human Ishikawa endometrial cancer cell migration and invasion through activation of ERK/mTOR signaling.

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