Cetrimonium Bromide Inhibits Cell Migration and Invasion of Human Hepatic SK-HEP-1 Cells Through Modulating the Canonical and Non-canonical TGF-β Signaling Pathways.
Identifieur interne : 000239 ( Main/Corpus ); précédent : 000238; suivant : 000240Cetrimonium Bromide Inhibits Cell Migration and Invasion of Human Hepatic SK-HEP-1 Cells Through Modulating the Canonical and Non-canonical TGF-β Signaling Pathways.
Auteurs : Tsai-Kun Wu ; Chung-Hung Chen ; Ying-Ru Pan ; Ching-Wen Hu ; Fu-Mei Huang ; Jer-Yuh Liu ; Chia-Jen LeeSource :
- Anticancer research [ 1791-7530 ] ; 2019.
English descriptors
- KwdEn :
- Adenocarcinoma (drug therapy), Adenocarcinoma (metabolism), Antineoplastic Agents (pharmacology), Cell Line, Tumor (MeSH), Cell Movement (drug effects), Cetrimonium (pharmacology), Humans (MeSH), Liver Neoplasms (drug therapy), Liver Neoplasms (metabolism), Neoplasm Invasiveness (MeSH), Signal Transduction (drug effects), Transforming Growth Factor beta (metabolism).
- MESH :
- chemical , metabolism : Transforming Growth Factor beta.
- chemical , pharmacology : Antineoplastic Agents, Cetrimonium.
- drug effects : Cell Movement, Signal Transduction.
- drug therapy : Adenocarcinoma, Liver Neoplasms.
- metabolism : Adenocarcinoma, Liver Neoplasms.
- Cell Line, Tumor, Humans, Neoplasm Invasiveness.
Abstract
BACKGROUND/AIM
Cetrimonium bromide (CTAB), a quaternary ammonium surfactant, is an antiseptic agent against bacteria and fungi. However, the mechanisms by which its pharmacological actions affect epithelial-mesenchymal transition (EMT) in hepatocellular carcinoma (HCC) cells, such as adenocarcinoma in SK-HEP-1 cells, have not been investigated. We, thereby, investigated whether CTAB inhibits cellular mobility and invasiveness of human hepatic adenocarcinoma in SK-HEP-1 cells.
MATERIALS AND METHODS
SK-HEP-1 cells were treated with CTAB, and subsequent migration and invasion were measured by wound healing and transwell assays. Protein expression was detected by immunoblotting analysis.
RESULTS
Our data revealed that treatment of SK-HEP-1 cells with CTAB altered their mesenchymal spindle-like morphology. CTAB exerted inhibitory effects on the migration and invasion of SK-HEP-1 cells dose-dependently, and reduced protein levels of matrix metalloproteinase-2 (MMP-2), MMP-9, snail, slug, twist, vimentin, fibronectin, N-cadherin, Smad2, Smad3, Smad4, phosphoinositide-3-kinase (PI3K), p-PI3K, Akt, p-Akt, β-catenin, mammalian target of rapamycin (mTOR), p-mTOR, p-p70S6K, p-extracellular signal-regulated kinases (ERK)1/2, p-p38 mitogen-activated protein kinase (MAPK) and p-c-Jun N-terminal kinase (JNK), but increased protein levels of tissue inhibitor matrix metalloproteinase-1 (TIMP-1), TIMP-2, claudin-1 and p-GSK3β. Based on these observations, we suggest that CTAB not only inhibits the canonical transforming growth factor-β (TGF-β) signaling pathway though reducing SMADs (an acronym from the fusion of Caenorhabditis elegans Sma genes and the Drosophila Mad, Mothers against decapentaplegic proteins), but also restrains the non-canonical TGF-β signaling including MAPK pathways like ERK1/2, p38 MAPK, JNK and PI3K.
CONCLUSION
CTAB is involved in the suppression of TGF-β-mediated mesenchymal phenotype and could be a potent medical agent for use in controlling the migration and invasion of hepatic adenocarcinoma.
DOI: 10.21873/anticanres.13510
PubMed: 31262888
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Chen</name><affiliation><nlm:affiliation>Department of Gastroenterology, Chang Bing Show Chwan Memorial Hospital, Changhua, Taiwan, R.O.C.</nlm:affiliation></affiliation></author><author><name sortKey="Pan, Ying Ru" sort="Pan, Ying Ru" uniqKey="Pan Y" first="Ying-Ru" last="Pan">Ying-Ru Pan</name><affiliation><nlm:affiliation>Department of Medical Research, Tungs' Taichung Metroharbor Hospital, Taichung, Taiwan, R.O.C.</nlm:affiliation></affiliation></author><author><name sortKey="Hu, Ching Wen" sort="Hu, Ching Wen" uniqKey="Hu C" first="Ching-Wen" last="Hu">Ching-Wen Hu</name><affiliation><nlm:affiliation>Department of Nursing, Tungs' Taichung Metroharbor Hospital, Taichung, Taiwan, R.O.C.</nlm:affiliation></affiliation></author><author><name sortKey="Huang, Fu Mei" sort="Huang, Fu Mei" uniqKey="Huang F" first="Fu-Mei" last="Huang">Fu-Mei Huang</name><affiliation><nlm:affiliation>Operating Theatre, Chung Shan Medical University Hospital, Taichung, Taiwan, R.O.C.</nlm:affiliation></affiliation></author><author><name sortKey="Liu, Jer Yuh" sort="Liu, Jer Yuh" uniqKey="Liu J" first="Jer-Yuh" last="Liu">Jer-Yuh Liu</name><affiliation><nlm:affiliation>Center for Molecular Medicine, China Medical University Hospital, Taichung, Taiwan, R.O.C.</nlm:affiliation></affiliation><affiliation><nlm:affiliation>Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan, R.O.C.</nlm:affiliation></affiliation></author><author><name sortKey="Lee, Chia Jen" sort="Lee, Chia Jen" uniqKey="Lee C" first="Chia-Jen" last="Lee">Chia-Jen Lee</name><affiliation><nlm:affiliation>Department of Medical Research, Tungs' Taichung Metroharbor Hospital, Taichung, Taiwan, R.O.C. chiajenlee54@gmail.com.</nlm:affiliation></affiliation><affiliation><nlm:affiliation>Department of Rehabilitation, Jen-Teh Junior College of Medicine, Nursing and Management, Miaoli, Taiwan R.O.C.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2019">2019</date><idno type="RBID">pubmed:31262888</idno><idno type="pmid">31262888</idno><idno type="doi">10.21873/anticanres.13510</idno><idno type="wicri:Area/Main/Corpus">000239</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000239</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Cetrimonium Bromide Inhibits Cell Migration and Invasion of Human Hepatic SK-HEP-1 Cells Through Modulating the Canonical and Non-canonical TGF-β Signaling Pathways.</title><author><name sortKey="Wu, Tsai Kun" sort="Wu, Tsai Kun" uniqKey="Wu T" first="Tsai-Kun" last="Wu">Tsai-Kun Wu</name><affiliation><nlm:affiliation>Division of Renal Medicine, Tungs' Taichung Metroharbor Hospital, Taichung, Taiwan, R.O.C.</nlm:affiliation></affiliation><affiliation><nlm:affiliation>Department of Nutrition, Master Program of Biomedical Nutrition, Hungkuang University, Taichung, Taiwan, R.O.C.</nlm:affiliation></affiliation><affiliation><nlm:affiliation>Department of Nursing, Jen-Teh Junior College of Medicine, Nursing and Management, Miaoli, Taiwan, R.O.C.</nlm:affiliation></affiliation></author><author><name sortKey="Chen, Chung Hung" sort="Chen, Chung Hung" uniqKey="Chen C" first="Chung-Hung" last="Chen">Chung-Hung Chen</name><affiliation><nlm:affiliation>Department of Gastroenterology, Chang Bing Show Chwan Memorial Hospital, Changhua, Taiwan, R.O.C.</nlm:affiliation></affiliation></author><author><name sortKey="Pan, Ying Ru" sort="Pan, Ying Ru" uniqKey="Pan Y" first="Ying-Ru" last="Pan">Ying-Ru Pan</name><affiliation><nlm:affiliation>Department of Medical Research, Tungs' Taichung Metroharbor Hospital, Taichung, Taiwan, R.O.C.</nlm:affiliation></affiliation></author><author><name sortKey="Hu, Ching Wen" sort="Hu, Ching Wen" uniqKey="Hu C" first="Ching-Wen" last="Hu">Ching-Wen Hu</name><affiliation><nlm:affiliation>Department of Nursing, Tungs' Taichung Metroharbor Hospital, Taichung, Taiwan, R.O.C.</nlm:affiliation></affiliation></author><author><name sortKey="Huang, Fu Mei" sort="Huang, Fu Mei" uniqKey="Huang F" first="Fu-Mei" last="Huang">Fu-Mei Huang</name><affiliation><nlm:affiliation>Operating Theatre, Chung Shan Medical University Hospital, Taichung, Taiwan, R.O.C.</nlm:affiliation></affiliation></author><author><name sortKey="Liu, Jer Yuh" sort="Liu, Jer Yuh" uniqKey="Liu J" first="Jer-Yuh" last="Liu">Jer-Yuh Liu</name><affiliation><nlm:affiliation>Center for Molecular Medicine, China Medical University Hospital, Taichung, Taiwan, R.O.C.</nlm:affiliation></affiliation><affiliation><nlm:affiliation>Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan, R.O.C.</nlm:affiliation></affiliation></author><author><name sortKey="Lee, Chia Jen" sort="Lee, Chia Jen" uniqKey="Lee C" first="Chia-Jen" last="Lee">Chia-Jen Lee</name><affiliation><nlm:affiliation>Department of Medical Research, Tungs' Taichung Metroharbor Hospital, Taichung, Taiwan, R.O.C. chiajenlee54@gmail.com.</nlm:affiliation></affiliation><affiliation><nlm:affiliation>Department of Rehabilitation, Jen-Teh Junior College of Medicine, Nursing and Management, Miaoli, Taiwan R.O.C.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Anticancer research</title><idno type="eISSN">1791-7530</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenocarcinoma (drug therapy)</term><term>Adenocarcinoma (metabolism)</term><term>Antineoplastic Agents (pharmacology)</term><term>Cell Line, Tumor (MeSH)</term><term>Cell Movement (drug effects)</term><term>Cetrimonium (pharmacology)</term><term>Humans (MeSH)</term><term>Liver Neoplasms (drug therapy)</term><term>Liver Neoplasms (metabolism)</term><term>Neoplasm Invasiveness (MeSH)</term><term>Signal Transduction (drug effects)</term><term>Transforming Growth Factor beta (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Transforming Growth Factor beta</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Agents</term><term>Cetrimonium</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Movement</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Adenocarcinoma</term><term>Liver Neoplasms</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Adenocarcinoma</term><term>Liver Neoplasms</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term><term>Humans</term><term>Neoplasm Invasiveness</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>BACKGROUND/AIM</b></p><p>Cetrimonium bromide (CTAB), a quaternary ammonium surfactant, is an antiseptic agent against bacteria and fungi. However, the mechanisms by which its pharmacological actions affect epithelial-mesenchymal transition (EMT) in hepatocellular carcinoma (HCC) cells, such as adenocarcinoma in SK-HEP-1 cells, have not been investigated. We, thereby, investigated whether CTAB inhibits cellular mobility and invasiveness of human hepatic adenocarcinoma in SK-HEP-1 cells.</p></div><div type="abstract" xml:lang="en"><p><b>MATERIALS AND METHODS</b></p><p>SK-HEP-1 cells were treated with CTAB, and subsequent migration and invasion were measured by wound healing and transwell assays. Protein expression was detected by immunoblotting analysis.</p></div><div type="abstract" xml:lang="en"><p><b>RESULTS</b></p><p>Our data revealed that treatment of SK-HEP-1 cells with CTAB altered their mesenchymal spindle-like morphology. CTAB exerted inhibitory effects on the migration and invasion of SK-HEP-1 cells dose-dependently, and reduced protein levels of matrix metalloproteinase-2 (MMP-2), MMP-9, snail, slug, twist, vimentin, fibronectin, N-cadherin, Smad2, Smad3, Smad4, phosphoinositide-3-kinase (PI3K), p-PI3K, Akt, p-Akt, β-catenin, mammalian target of rapamycin (mTOR), p-mTOR, p-p70S6K, p-extracellular signal-regulated kinases (ERK)1/2, p-p38 mitogen-activated protein kinase (MAPK) and p-c-Jun N-terminal kinase (JNK), but increased protein levels of tissue inhibitor matrix metalloproteinase-1 (TIMP-1), TIMP-2, claudin-1 and p-GSK3β. Based on these observations, we suggest that CTAB not only inhibits the canonical transforming growth factor-β (TGF-β) signaling pathway though reducing SMADs (an acronym from the fusion of Caenorhabditis elegans Sma genes and the Drosophila Mad, Mothers against decapentaplegic proteins), but also restrains the non-canonical TGF-β signaling including MAPK pathways like ERK1/2, p38 MAPK, JNK and PI3K.</p></div><div type="abstract" xml:lang="en"><p><b>CONCLUSION</b></p><p>CTAB is involved in the suppression of TGF-β-mediated mesenchymal phenotype and could be a potent medical agent for use in controlling the migration and invasion of hepatic adenocarcinoma.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31262888</PMID><DateCompleted><Year>2019</Year><Month>07</Month><Day>08</Day></DateCompleted><DateRevised><Year>2019</Year><Month>07</Month><Day>08</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1791-7530</ISSN><JournalIssue CitedMedium="Internet"><Volume>39</Volume><Issue>7</Issue><PubDate><Year>2019</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Anticancer research</Title><ISOAbbreviation>Anticancer Res</ISOAbbreviation></Journal><ArticleTitle>Cetrimonium Bromide Inhibits Cell Migration and Invasion of Human Hepatic SK-HEP-1 Cells Through Modulating the Canonical and Non-canonical TGF-β Signaling Pathways.</ArticleTitle><Pagination><MedlinePgn>3621-3631</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.21873/anticanres.13510</ELocationID><Abstract><AbstractText Label="BACKGROUND/AIM" NlmCategory="OBJECTIVE">Cetrimonium bromide (CTAB), a quaternary ammonium surfactant, is an antiseptic agent against bacteria and fungi. However, the mechanisms by which its pharmacological actions affect epithelial-mesenchymal transition (EMT) in hepatocellular carcinoma (HCC) cells, such as adenocarcinoma in SK-HEP-1 cells, have not been investigated. We, thereby, investigated whether CTAB inhibits cellular mobility and invasiveness of human hepatic adenocarcinoma in SK-HEP-1 cells.</AbstractText><AbstractText Label="MATERIALS AND METHODS" NlmCategory="METHODS">SK-HEP-1 cells were treated with CTAB, and subsequent migration and invasion were measured by wound healing and transwell assays. Protein expression was detected by immunoblotting analysis.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Our data revealed that treatment of SK-HEP-1 cells with CTAB altered their mesenchymal spindle-like morphology. CTAB exerted inhibitory effects on the migration and invasion of SK-HEP-1 cells dose-dependently, and reduced protein levels of matrix metalloproteinase-2 (MMP-2), MMP-9, snail, slug, twist, vimentin, fibronectin, N-cadherin, Smad2, Smad3, Smad4, phosphoinositide-3-kinase (PI3K), p-PI3K, Akt, p-Akt, β-catenin, mammalian target of rapamycin (mTOR), p-mTOR, p-p70S6K, p-extracellular signal-regulated kinases (ERK)1/2, p-p38 mitogen-activated protein kinase (MAPK) and p-c-Jun N-terminal kinase (JNK), but increased protein levels of tissue inhibitor matrix metalloproteinase-1 (TIMP-1), TIMP-2, claudin-1 and p-GSK3β. Based on these observations, we suggest that CTAB not only inhibits the canonical transforming growth factor-β (TGF-β) signaling pathway though reducing SMADs (an acronym from the fusion of Caenorhabditis elegans Sma genes and the Drosophila Mad, Mothers against decapentaplegic proteins), but also restrains the non-canonical TGF-β signaling including MAPK pathways like ERK1/2, p38 MAPK, JNK and PI3K.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">CTAB is involved in the suppression of TGF-β-mediated mesenchymal phenotype and could be a potent medical agent for use in controlling the migration and invasion of hepatic adenocarcinoma.</AbstractText><CopyrightInformation>Copyright© 2019, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wu</LastName><ForeName>Tsai-Kun</ForeName><Initials>TK</Initials><AffiliationInfo><Affiliation>Division of Renal Medicine, Tungs' Taichung Metroharbor Hospital, Taichung, Taiwan, R.O.C.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Nutrition, Master Program of Biomedical Nutrition, Hungkuang University, Taichung, Taiwan, R.O.C.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Nursing, Jen-Teh Junior College of Medicine, Nursing and Management, Miaoli, Taiwan, R.O.C.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Chung-Hung</ForeName><Initials>CH</Initials><AffiliationInfo><Affiliation>Department of Gastroenterology, Chang Bing Show Chwan Memorial Hospital, Changhua, Taiwan, R.O.C.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pan</LastName><ForeName>Ying-Ru</ForeName><Initials>YR</Initials><AffiliationInfo><Affiliation>Department of Medical Research, Tungs' Taichung Metroharbor Hospital, Taichung, Taiwan, R.O.C.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hu</LastName><ForeName>Ching-Wen</ForeName><Initials>CW</Initials><AffiliationInfo><Affiliation>Department of Nursing, Tungs' Taichung Metroharbor Hospital, Taichung, Taiwan, R.O.C.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Fu-Mei</ForeName><Initials>FM</Initials><AffiliationInfo><Affiliation>Operating Theatre, Chung Shan Medical University Hospital, Taichung, Taiwan, R.O.C.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Jer-Yuh</ForeName><Initials>JY</Initials><AffiliationInfo><Affiliation>Center for Molecular Medicine, China Medical University Hospital, Taichung, Taiwan, R.O.C.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan, R.O.C.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Chia-Jen</ForeName><Initials>CJ</Initials><AffiliationInfo><Affiliation>Department of Medical Research, Tungs' Taichung Metroharbor Hospital, Taichung, Taiwan, R.O.C. chiajenlee54@gmail.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Rehabilitation, Jen-Teh Junior College of Medicine, Nursing and Management, Miaoli, Taiwan R.O.C.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Greece</Country><MedlineTA>Anticancer Res</MedlineTA><NlmUniqueID>8102988</NlmUniqueID><ISSNLinking>0250-7005</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000970">Antineoplastic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016212">Transforming Growth Factor beta</NameOfSubstance></Chemical><Chemical><RegistryNumber>Z7FF1XKL7A</RegistryNumber><NameOfSubstance UI="D000077286">Cetrimonium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000230" MajorTopicYN="N">Adenocarcinoma</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000970" MajorTopicYN="N">Antineoplastic Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002465" MajorTopicYN="N">Cell Movement</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000077286" MajorTopicYN="N">Cetrimonium</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008113" MajorTopicYN="N">Liver Neoplasms</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009361" MajorTopicYN="N">Neoplasm Invasiveness</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016212" MajorTopicYN="N">Transforming Growth Factor beta</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Cetrimonium bromide (CTAB)</Keyword><Keyword MajorTopicYN="N">SK-HEP-1</Keyword><Keyword MajorTopicYN="N">hepatic cancer</Keyword><Keyword MajorTopicYN="N">transforming growth factor-β (TGF-β)</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>05</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2019</Year><Month>06</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>06</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>7</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>7</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>7</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31262888</ArticleId><ArticleId IdType="pii">39/7/3621</ArticleId><ArticleId IdType="doi">10.21873/anticanres.13510</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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