ChloroquineV1, PubMed, Checkpoint, bibRecord, 000101

JTC801 Induces pH-dependent Death Specifically in Cancer Cells and Slows Growth of Tumors in Mice.

Identifieur interne : 000101 ( PubMed/Checkpoint ); précédent : 000100; suivant : 000102

JTC801 Induces pH-dependent Death Specifically in Cancer Cells and Slows Growth of Tumors in Mice.

Auteurs : Xinxin Song [États-Unis] ; Shan Zhu [République populaire de Chine] ; Yangchun Xie [États-Unis] ; Jiao Liu [République populaire de Chine] ; Lingyi Sun [États-Unis] ; Dexing Zeng [États-Unis] ; Pengcheng Wang [États-Unis] ; Xiaochao Ma [États-Unis] ; Guido Kroemer [Suède] ; David L. Bartlett [États-Unis] ; Timothy R. Billiar [États-Unis] ; Michael T. Lotze [États-Unis] ; Herbert J. Zeh [États-Unis] ; Rui Kang [États-Unis] ; Daolin Tang [États-Unis]

Source :

Gastroenterology [ 1528-0012 ] ; 2018.

RBID : pubmed:29248440

Descripteurs français

English descriptors

KwdEn :
- Adenocarcinoma (drug therapy), Adenocarcinoma (genetics), Adenocarcinoma (metabolism), Adenocarcinoma (secondary), Aminoquinolines (pharmacology), Animals, Antigens, Neoplasm (metabolism), Antineoplastic Agents (pharmacology), Benzamides (pharmacology), Biomarkers, Tumor (genetics), Biomarkers, Tumor (metabolism), Carbonic Anhydrase IX (metabolism), Cell Death (drug effects), Dose-Response Relationship, Drug, Female, Gene Expression Regulation, Neoplastic, HCT116 Cells, Humans, Hydrogen-Ion Concentration, Mice, Inbred C57BL, Mice, Nude, NF-kappa B (metabolism), Neoplastic Stem Cells (drug effects), Neoplastic Stem Cells (metabolism), Neoplastic Stem Cells (pathology), Pancreatic Neoplasms (drug therapy), Pancreatic Neoplasms (genetics), Pancreatic Neoplasms (metabolism), Pancreatic Neoplasms (pathology), Signal Transduction (drug effects), Time Factors, Tumor Burden (drug effects), Tumor Microenvironment, Xenograft Model Antitumor Assays.
MESH :
- chemical , genetics : Biomarkers, Tumor.
- chemical , metabolism : Antigens, Neoplasm, Biomarkers, Tumor, Carbonic Anhydrase IX, NF-kappa B.
- chemical , pharmacology : Aminoquinolines, Antineoplastic Agents, Benzamides.
- drug effects : Cell Death, Neoplastic Stem Cells, Signal Transduction, Tumor Burden.
- drug therapy : Adenocarcinoma, Pancreatic Neoplasms.
- genetics : Adenocarcinoma, Pancreatic Neoplasms.
- metabolism : Adenocarcinoma, Neoplastic Stem Cells, Pancreatic Neoplasms.
- pathology : Neoplastic Stem Cells, Pancreatic Neoplasms.
- secondary : Adenocarcinoma.
- Animals, Dose-Response Relationship, Drug, Female, Gene Expression Regulation, Neoplastic, HCT116 Cells, Humans, Hydrogen-Ion Concentration, Mice, Inbred C57BL, Mice, Nude, Time Factors, Tumor Microenvironment, Xenograft Model Antitumor Assays.

Abstract

Maintenance of acid-base homeostasis is required for normal physiology, metabolism, and development. It is not clear how cell death is activated in response to changes in pH. We performed a screen to identify agents that induce cell death in a pH-dependent manner (we call this alkaliptosis) in pancreatic ductal adenocarcinoma cancer (PDAC) cells and tested their effects in mice.

DOI: 10.1053/j.gastro.2017.12.004
PubMed: 29248440

Affiliations:

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Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenocarcinoma (drug therapy)</term>
<term>Adenocarcinoma (genetics)</term>
<term>Adenocarcinoma (metabolism)</term>
<term>Adenocarcinoma (secondary)</term>
<term>Aminoquinolines (pharmacology)</term>
<term>Animals</term>
<term>Antigens, Neoplasm (metabolism)</term>
<term>Antineoplastic Agents (pharmacology)</term>
<term>Benzamides (pharmacology)</term>
<term>Biomarkers, Tumor (genetics)</term>
<term>Biomarkers, Tumor (metabolism)</term>
<term>Carbonic Anhydrase IX (metabolism)</term>
<term>Cell Death (drug effects)</term>
<term>Dose-Response Relationship, Drug</term>
<term>Female</term>
<term>Gene Expression Regulation, Neoplastic</term>
<term>HCT116 Cells</term>
<term>Humans</term>
<term>Hydrogen-Ion Concentration</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Nude</term>
<term>NF-kappa B (metabolism)</term>
<term>Neoplastic Stem Cells (drug effects)</term>
<term>Neoplastic Stem Cells (metabolism)</term>
<term>Neoplastic Stem Cells (pathology)</term>
<term>Pancreatic Neoplasms (drug therapy)</term>
<term>Pancreatic Neoplasms (genetics)</term>
<term>Pancreatic Neoplasms (metabolism)</term>
<term>Pancreatic Neoplasms (pathology)</term>
<term>Signal Transduction (drug effects)</term>
<term>Time Factors</term>
<term>Tumor Burden (drug effects)</term>
<term>Tumor Microenvironment</term>
<term>Xenograft Model Antitumor Assays</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Adénocarcinome (génétique)</term>
<term>Adénocarcinome (métabolisme)</term>
<term>Adénocarcinome (secondaire)</term>
<term>Adénocarcinome (traitement médicamenteux)</term>
<term>Aminoquinoléines (pharmacologie)</term>
<term>Animaux</term>
<term>Antigènes néoplasiques (métabolisme)</term>
<term>Antinéoplasiques (pharmacologie)</term>
<term>Benzamides (pharmacologie)</term>
<term>Carbonic anhydrase IX (métabolisme)</term>
<term>Cellules HCT116</term>
<term>Cellules souches tumorales ()</term>
<term>Cellules souches tumorales (anatomopathologie)</term>
<term>Cellules souches tumorales (métabolisme)</term>
<term>Charge tumorale ()</term>
<term>Concentration en ions d'hydrogène</term>
<term>Facteur de transcription NF-kappa B (métabolisme)</term>
<term>Facteurs temps</term>
<term>Femelle</term>
<term>Humains</term>
<term>Marqueurs biologiques tumoraux (génétique)</term>
<term>Marqueurs biologiques tumoraux (métabolisme)</term>
<term>Microenvironnement tumoral</term>
<term>Mort cellulaire ()</term>
<term>Relation dose-effet des médicaments</term>
<term>Régulation de l'expression des gènes tumoraux</term>
<term>Souris de lignée C57BL</term>
<term>Souris nude</term>
<term>Tests d'activité antitumorale sur modèle de xénogreffe</term>
<term>Transduction du signal ()</term>
<term>Tumeurs du pancréas (anatomopathologie)</term>
<term>Tumeurs du pancréas (génétique)</term>
<term>Tumeurs du pancréas (métabolisme)</term>
<term>Tumeurs du pancréas (traitement médicamenteux)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Biomarkers, Tumor</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Antigens, Neoplasm</term>
<term>Biomarkers, Tumor</term>
<term>Carbonic Anhydrase IX</term>
<term>NF-kappa B</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Aminoquinolines</term>
<term>Antineoplastic Agents</term>
<term>Benzamides</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Cellules souches tumorales</term>
<term>Tumeurs du pancréas</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Death</term>
<term>Neoplastic Stem Cells</term>
<term>Signal Transduction</term>
<term>Tumor Burden</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Adenocarcinoma</term>
<term>Pancreatic Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Adenocarcinoma</term>
<term>Pancreatic Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Adénocarcinome</term>
<term>Marqueurs biologiques tumoraux</term>
<term>Tumeurs du pancréas</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Adenocarcinoma</term>
<term>Neoplastic Stem Cells</term>
<term>Pancreatic Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Adénocarcinome</term>
<term>Antigènes néoplasiques</term>
<term>Carbonic anhydrase IX</term>
<term>Cellules souches tumorales</term>
<term>Facteur de transcription NF-kappa B</term>
<term>Marqueurs biologiques tumoraux</term>
<term>Tumeurs du pancréas</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neoplastic Stem Cells</term>
<term>Pancreatic Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Aminoquinoléines</term>
<term>Antinéoplasiques</term>
<term>Benzamides</term>
</keywords>
<keywords scheme="MESH" qualifier="secondaire" xml:lang="fr"><term>Adénocarcinome</term>
</keywords>
<keywords scheme="MESH" qualifier="secondary" xml:lang="en"><term>Adenocarcinoma</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Adénocarcinome</term>
<term>Tumeurs du pancréas</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Dose-Response Relationship, Drug</term>
<term>Female</term>
<term>Gene Expression Regulation, Neoplastic</term>
<term>HCT116 Cells</term>
<term>Humans</term>
<term>Hydrogen-Ion Concentration</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Nude</term>
<term>Time Factors</term>
<term>Tumor Microenvironment</term>
<term>Xenograft Model Antitumor Assays</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Cellules HCT116</term>
<term>Cellules souches tumorales</term>
<term>Charge tumorale</term>
<term>Concentration en ions d'hydrogène</term>
<term>Facteurs temps</term>
<term>Femelle</term>
<term>Humains</term>
<term>Microenvironnement tumoral</term>
<term>Mort cellulaire</term>
<term>Relation dose-effet des médicaments</term>
<term>Régulation de l'expression des gènes tumoraux</term>
<term>Souris de lignée C57BL</term>
<term>Souris nude</term>
<term>Tests d'activité antitumorale sur modèle de xénogreffe</term>
<term>Transduction du signal</term>
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<front><div type="abstract" xml:lang="en">Maintenance of acid-base homeostasis is required for normal physiology, metabolism, and development. It is not clear how cell death is activated in response to changes in pH. We performed a screen to identify agents that induce cell death in a pH-dependent manner (we call this alkaliptosis) in pancreatic ductal adenocarcinoma cancer (PDAC) cells and tested their effects in mice.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29248440</PMID>
<DateCompleted><Year>2018</Year>
<Month>05</Month>
<Day>09</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>04</Month>
<Day>01</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1528-0012</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>154</Volume>
<Issue>5</Issue>
<PubDate><Year>2018</Year>
<Month>04</Month>
</PubDate>
</JournalIssue>
<Title>Gastroenterology</Title>
<ISOAbbreviation>Gastroenterology</ISOAbbreviation>
</Journal>
<ArticleTitle>JTC801 Induces pH-dependent Death Specifically in Cancer Cells and Slows Growth of Tumors in Mice.</ArticleTitle>
<Pagination><MedlinePgn>1480-1493</MedlinePgn>
</Pagination>
<ELocationID EIdType="pii" ValidYN="Y">S0016-5085(17)36696-9</ELocationID>
<ELocationID EIdType="doi" ValidYN="Y">10.1053/j.gastro.2017.12.004</ELocationID>
<Abstract><AbstractText Label="BACKGROUND & AIMS">Maintenance of acid-base homeostasis is required for normal physiology, metabolism, and development. It is not clear how cell death is activated in response to changes in pH. We performed a screen to identify agents that induce cell death in a pH-dependent manner (we call this alkaliptosis) in pancreatic ductal adenocarcinoma cancer (PDAC) cells and tested their effects in mice.</AbstractText>
<AbstractText Label="METHODS">We screened a library of 254 compounds that interact with G-protein-coupled receptors (GPCRs) to identify those with cytotoxic activity against a human PDAC cell line (PANC1). We evaluated the ability of JTC801, which binds the opiod receptor and has analgesic effects, to stimulate cell death in human PDAC cell lines (PANC1, MiaPaCa2, CFPAC1, PANC2.03, BxPc3, and CAPAN2), mouse pancreatic cancer-associated stellate cell lines, primary human pancreatic ductal epithelial cells, and 60 cancer cell lines (the NCI-60 panel). Genes encoding proteins in cell death and GPCR signaling pathways, as well as those that regulate nuclear factor-κB (NF-κB) activity, were knocked out, knocked down, or expressed from transgenes in cancer cell lines. JTC801 was administered by gavage to mice with xenograft tumors, C57BL/6 mice with orthographic pancreatic tumors grown from Pdx1-Cre;KRas<sup>G12D/+</sup>
;Tp53<sup>R172H/+</sup>
 (KPC) cells, mice with metastases following tail-vein injection of KPC cells, and Pdx-1-Cre;Kras<sup>G12D/+</sup>
 mice crossed with Hmgb1<sup>flox/flox</sup>
 mice (KCH mice). Pancreata were collected from mice and analyzed for tumor growth and by histology and immunohistochemistry. We compared gene and protein expression levels between human pancreatic cancer tissues and patient survival times using online R2 genomic or immunohistochemistry analyses.</AbstractText>
<AbstractText Label="RESULTS">Exposure of human PDAC cell lines (PANC1 and MiaPaCa2) to JTC801 did not induce molecular markers of apoptosis (cleavage of caspase 3 or poly [ADP ribose] polymerase [PARP]), necroptosis (interaction between receptor-interacting serine-threonine kinase 3 [RIPK3] and mixed lineage kinase domain like pseudokinase [MLKL]), or ferroptosis (degradation of glutathione peroxidase 4 [GPX4]). Inhibitors of apoptosis (Z-VAD-FMK), necroptosis (necrosulfonamide), ferroptosis (ferrostatin-1), or autophagy (hydroxychloroquine) did not prevent JTC801-induced death of PANC1 or MiaPaCa2 cells. The cytotoxic effects of JTC801 in immortalized fibroblast cell lines was not affected by disruption of genes that promote apoptosis (Bax<sup>-/-</sup>
/Bak<sup>-/-</sup>
 cells), necroptosis (Ripk1<sup>-/-</sup>
, Ripk3<sup>-/-</sup>
, or Mlkl<sup>-/-</sup>
 cells), ferroptosis (Gpx4<sup>-/-</sup>
 cells), or autophagy (Atg3<sup>-/-</sup>
, Atg5<sup>-/-</sup>
, Atg7<sup>-/-</sup>
, or Sqstm1<sup>-/-</sup>
 cells). We found JTC801 to induce a pH-dependent form cell death (alkaliptosis) in cancer cells but not normal cells (hepatocytes, bone marrow CD34<sup>+</sup>
 progenitor cells, peripheral blood mononuclear cells, or dermal fibroblasts) or healthy tissues of C57BL/6 mice. JTC801 induced alkaliptosis in cancer cells by activating NF-κB, which repressed expression of the carbonic anhydrase 9 gene (CA9), whose product regulates pH balance in cells. In analyses of Cancer Genome Atlas data and tissue microarrays, we associated increased tumor level of CA9 mRNA or protein with shorter survival times of patients with pancreatic, kidney, or lung cancers. Knockdown of CA9 reduced the protective effects of NF-κB inhibition on JTC801-induced cell death and intracellular alkalinization in PANC1 and MiaPaCa2 cell lines. Oral administration of JTC801 inhibited growth of xenograft tumors (from PANC1, MiaPaCa2, SK-MEL-28, PC-3, 786-0, SF-295, HCT116, OV-CAR3, and HuH7 cells), orthotropic tumors (from KPC cells), lung metastases (from KPC cells) of mice, and slowed growth of tumors in KCH mice.</AbstractText>
<AbstractText Label="CONCLUSIONS">In a screen of agents that interact with GPCR pathways, we found JTC801 to induce pH-dependent cell death (alkaliptosis) specifically in cancer cells such as PDAC cells, by reducing expression of CA9. Levels of CA9 are increased in human cancer tissues. JTC801 might be developed for treatment of pancreatic cancer.</AbstractText>
<CopyrightInformation>Copyright © 2018 AGA Institute. Published by Elsevier Inc. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Song</LastName>
<ForeName>Xinxin</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>The Third Affiliated Hospital, Center for DAMP Biology, Key Laboratory for Major Obstetric Diseases of Guangdong Province, Key Laboratory of Protein Modification and Degradation of Guangdong Higher Education Institutes, Key Laboratory of Reproduction and Genetics of Guangdong Higher Education Institutes, Guangzhou Medical University, Guangzhou, Guangdong, 510510, China; Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhu</LastName>
<ForeName>Shan</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>The Third Affiliated Hospital, Center for DAMP Biology, Key Laboratory for Major Obstetric Diseases of Guangdong Province, Key Laboratory of Protein Modification and Degradation of Guangdong Higher Education Institutes, Key Laboratory of Reproduction and Genetics of Guangdong Higher Education Institutes, Guangzhou Medical University, Guangzhou, Guangdong, 510510, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xie</LastName>
<ForeName>Yangchun</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Jiao</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>The Third Affiliated Hospital, Center for DAMP Biology, Key Laboratory for Major Obstetric Diseases of Guangdong Province, Key Laboratory of Protein Modification and Degradation of Guangdong Higher Education Institutes, Key Laboratory of Reproduction and Genetics of Guangdong Higher Education Institutes, Guangzhou Medical University, Guangzhou, Guangdong, 510510, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sun</LastName>
<ForeName>Lingyi</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zeng</LastName>
<ForeName>Dexing</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Pengcheng</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>Department of Pharmaceutical Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ma</LastName>
<ForeName>Xiaochao</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Department of Pharmaceutical Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kroemer</LastName>
<ForeName>Guido</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>Université Paris Descartes, Sorbonne Paris Cité, Paris, France; Equipe 11 labellisée Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, Paris, France; Institut National de la Santé et de la Recherche Médicale, Paris, France; Université Pierre et Marie Curie, Paris, France; Metabolomics and Cell Biology Platforms, Gustave Roussy Cancer Campus, Villejuif, France; Pôle de Biologie, Hôpital Européen Georges Pompidou, AP-HP, Paris, France; Department of Women's and Children's Health, Karolinska University Hospital, Stockholm, Sweden.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Bartlett</LastName>
<ForeName>David L</ForeName>
<Initials>DL</Initials>
<AffiliationInfo><Affiliation>Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Billiar</LastName>
<ForeName>Timothy R</ForeName>
<Initials>TR</Initials>
<AffiliationInfo><Affiliation>Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lotze</LastName>
<ForeName>Michael T</ForeName>
<Initials>MT</Initials>
<AffiliationInfo><Affiliation>Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zeh</LastName>
<ForeName>Herbert J</ForeName>
<Initials>HJ</Initials>
<AffiliationInfo><Affiliation>Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kang</LastName>
<ForeName>Rui</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Tang</LastName>
<ForeName>Daolin</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>The Third Affiliated Hospital, Center for DAMP Biology, Key Laboratory for Major Obstetric Diseases of Guangdong Province, Key Laboratory of Protein Modification and Degradation of Guangdong Higher Education Institutes, Key Laboratory of Reproduction and Genetics of Guangdong Higher Education Institutes, Guangzhou Medical University, Guangzhou, Guangdong, 510510, China; Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania. Electronic address: tangd2@upmc.edu.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>R01 CA211070</GrantID>
<Acronym>CA</Acronym>
<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 CA181450</GrantID>
<Acronym>CA</Acronym>
<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>P30 CA047904</GrantID>
<Acronym>CA</Acronym>
<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 GM115366</GrantID>
<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 CA160417</GrantID>
<Acronym>CA</Acronym>
<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2017</Year>
<Month>12</Month>
<Day>14</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Gastroenterology</MedlineTA>
<NlmUniqueID>0374630</NlmUniqueID>
<ISSNLinking>0016-5085</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000634">Aminoquinolines</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000951">Antigens, Neoplasm</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000970">Antineoplastic Agents</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D001549">Benzamides</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D014408">Biomarkers, Tumor</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C433236">N-(4-amino-2-methylquinolin-6-yl)-2-(4-ethylphenoxymethyl)benzamide</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D016328">NF-kappa B</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 4.2.1.1</RegistryNumber>
<NameOfSubstance UI="C089226">CA9 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 4.2.1.1</RegistryNumber>
<NameOfSubstance UI="D000071231">Carbonic Anhydrase IX</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 4.2.1.1.</RegistryNumber>
<NameOfSubstance UI="C492796">Car9 protein, mouse</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>AIM</CitationSubset>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000230" MajorTopicYN="N">Adenocarcinoma</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000556" MajorTopicYN="N">secondary</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000634" MajorTopicYN="N">Aminoquinolines</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000951" MajorTopicYN="N">Antigens, Neoplasm</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000970" MajorTopicYN="N">Antineoplastic Agents</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001549" MajorTopicYN="N">Benzamides</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014408" MajorTopicYN="N">Biomarkers, Tumor</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071231" MajorTopicYN="N">Carbonic Anhydrase IX</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D016923" MajorTopicYN="N">Cell Death</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004305" MajorTopicYN="N">Dose-Response Relationship, Drug</DescriptorName>
</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="D045325" MajorTopicYN="N">HCT116 Cells</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006863" MajorTopicYN="N">Hydrogen-Ion Concentration</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008819" MajorTopicYN="N">Mice, Nude</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D016328" MajorTopicYN="N">NF-kappa B</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014411" MajorTopicYN="N">Neoplastic Stem Cells</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010190" MajorTopicYN="N">Pancreatic Neoplasms</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
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JTC801 Induces pH-dependent Death Specifically in Cancer Cells and Slows Growth of Tumors in Mice.

JTC801 Induces pH-dependent Death Specifically in Cancer Cells and Slows Growth of Tumors in Mice.

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