The triazole linked galactose substituted dicyano compound can induce autophagy in NSCLC cell lines.
Identifieur interne : 000048 ( PubMed/Corpus ); précédent : 000047; suivant : 000049The triazole linked galactose substituted dicyano compound can induce autophagy in NSCLC cell lines.
Auteurs : Ozge Alvur ; Onur Tokgun ; Yasemin Baygu ; Nilgun Kabay ; Yasar Gok ; Hakan AkcaSource :
- Gene [ 1879-0038 ] ; 2019.
English descriptors
- KwdEn :
- Adaptor Proteins, Signal Transducing (metabolism), Antineoplastic Agents, Apoptosis, Apoptosis Regulatory Proteins (metabolism), Autophagy, Carcinoma, Non-Small-Cell Lung (drug therapy), Carcinoma, Non-Small-Cell Lung (metabolism), Cell Line, Tumor, Cell Proliferation (drug effects), Cell Survival (drug effects), Chloroquine (chemistry), Drug Resistance, Neoplasm, Drug Screening Assays, Antitumor, Galactose (chemistry), Humans, Inhibitory Concentration 50, Lung Neoplasms (drug therapy), Lung Neoplasms (metabolism), Microscopy, Electron, Transmission, Microtubule-Associated Proteins (metabolism), Naphthyridines (metabolism), Signal Transduction (drug effects), TOR Serine-Threonine Kinases (metabolism), Triazoles (chemistry).
- MESH :
- chemical , chemistry : Chloroquine, Galactose, Triazoles.
- chemical , metabolism : Adaptor Proteins, Signal Transducing, Apoptosis Regulatory Proteins, Microtubule-Associated Proteins, Naphthyridines, TOR Serine-Threonine Kinases.
- chemical : Antineoplastic Agents.
- drug effects : Cell Proliferation, Cell Survival, Signal Transduction.
- drug therapy : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- metabolism : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- Apoptosis, Autophagy, Cell Line, Tumor, Drug Resistance, Neoplasm, Drug Screening Assays, Antitumor, Humans, Inhibitory Concentration 50, Microscopy, Electron, Transmission.
Abstract
As seen in other types of cancer, development of drug resistance in NSCLC treatment causes adverse effects on disease fighting process. Recent studies have shown that one of the drug resistance development mechanisms is that cancer cells may acquire the ability to escape from cell death. Therefore, development of anticancer drugs which have the strategy to redirect cancer cells to any cell death pathways may provide positive results for cancer treatments. Autophagy may be a target mechanism of alternative cancer treatment strategy in cases of blocked apoptosis. There is also a complex molecular link between autophagy and apoptosis, has not been fully understood yet. The dicyano compound which we used in our study caused cell death in NSCLC cell lines. When we analyzed the cells which were treated with dicyano compound by transmission electron microscope, we observed autophagosome structures. Upon this result, we investigated expression levels of autophagic proteins in the dicyano compound-treated cells by immunoblotting and observed that expression levels of autophagic proteins were increased significantly. The TUNEL assay and qRT-PCR for pro-apoptotic and anti-apoptotic gene expression, which we performed to assess apoptosis in the dicyano compound-treated cells, showed that the cell death does not occur through apoptotic pathway. We showed that the dicyano compound, which was developed in our laboratories, may play a role in molecular link between apoptosis and autophagy and may shed light on development of new anticancer treatment strategies.
DOI: 10.1016/j.gene.2019.06.025
PubMed: 31247220
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pubmed:31247220Le document en format XML
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Electronic address: hakca@pau.edu.tr.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2019">2019</date><idno type="RBID">pubmed:31247220</idno><idno type="pmid">31247220</idno><idno type="doi">10.1016/j.gene.2019.06.025</idno><idno type="wicri:Area/PubMed/Corpus">000048</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000048</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">The triazole linked galactose substituted dicyano compound can induce autophagy in NSCLC cell lines.</title><author><name sortKey="Alvur, Ozge" sort="Alvur, Ozge" uniqKey="Alvur O" first="Ozge" last="Alvur">Ozge Alvur</name><affiliation><nlm:affiliation>Department of Medical Biology, Pamukkale University, Denizli, Turkey; Department of Medical Biology, Van Yuzuncu Yil University, Van, Turkey.</nlm:affiliation></affiliation></author><author><name sortKey="Tokgun, Onur" sort="Tokgun, Onur" uniqKey="Tokgun O" first="Onur" last="Tokgun">Onur Tokgun</name><affiliation><nlm:affiliation>Department of Medical Genetics, Pamukkale University, Denizli, Turkey.</nlm:affiliation></affiliation></author><author><name sortKey="Baygu, Yasemin" sort="Baygu, Yasemin" uniqKey="Baygu Y" first="Yasemin" last="Baygu">Yasemin Baygu</name><affiliation><nlm:affiliation>Department of Chemistry, Pamukkale University, Denizli, Turkey.</nlm:affiliation></affiliation></author><author><name sortKey="Kabay, Nilgun" sort="Kabay, Nilgun" uniqKey="Kabay N" first="Nilgun" last="Kabay">Nilgun Kabay</name><affiliation><nlm:affiliation>Department of Biomedical Engineering, Pamukkale University, Denizli, Turkey.</nlm:affiliation></affiliation></author><author><name sortKey="Gok, Yasar" sort="Gok, Yasar" uniqKey="Gok Y" first="Yasar" last="Gok">Yasar Gok</name><affiliation><nlm:affiliation>Department of Chemical Engineering, Usak University, Usak, Turkey.</nlm:affiliation></affiliation></author><author><name sortKey="Akca, Hakan" sort="Akca, Hakan" uniqKey="Akca H" first="Hakan" last="Akca">Hakan Akca</name><affiliation><nlm:affiliation>Department of Medical Genetics, Pamukkale University, Denizli, Turkey. Electronic address: hakca@pau.edu.tr.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Gene</title><idno type="eISSN">1879-0038</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adaptor Proteins, Signal Transducing (metabolism)</term><term>Antineoplastic Agents</term><term>Apoptosis</term><term>Apoptosis Regulatory Proteins (metabolism)</term><term>Autophagy</term><term>Carcinoma, Non-Small-Cell Lung (drug therapy)</term><term>Carcinoma, Non-Small-Cell Lung (metabolism)</term><term>Cell Line, Tumor</term><term>Cell Proliferation (drug effects)</term><term>Cell Survival (drug effects)</term><term>Chloroquine (chemistry)</term><term>Drug Resistance, Neoplasm</term><term>Drug Screening Assays, Antitumor</term><term>Galactose (chemistry)</term><term>Humans</term><term>Inhibitory Concentration 50</term><term>Lung Neoplasms (drug therapy)</term><term>Lung Neoplasms (metabolism)</term><term>Microscopy, Electron, Transmission</term><term>Microtubule-Associated Proteins (metabolism)</term><term>Naphthyridines (metabolism)</term><term>Signal Transduction (drug effects)</term><term>TOR Serine-Threonine Kinases (metabolism)</term><term>Triazoles (chemistry)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Chloroquine</term><term>Galactose</term><term>Triazoles</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adaptor Proteins, Signal Transducing</term><term>Apoptosis Regulatory Proteins</term><term>Microtubule-Associated Proteins</term><term>Naphthyridines</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Antineoplastic Agents</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Proliferation</term><term>Cell Survival</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term><term>Cell Line, Tumor</term><term>Drug Resistance, Neoplasm</term><term>Drug Screening Assays, Antitumor</term><term>Humans</term><term>Inhibitory Concentration 50</term><term>Microscopy, Electron, Transmission</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">As seen in other types of cancer, development of drug resistance in NSCLC treatment causes adverse effects on disease fighting process. Recent studies have shown that one of the drug resistance development mechanisms is that cancer cells may acquire the ability to escape from cell death. Therefore, development of anticancer drugs which have the strategy to redirect cancer cells to any cell death pathways may provide positive results for cancer treatments. Autophagy may be a target mechanism of alternative cancer treatment strategy in cases of blocked apoptosis. There is also a complex molecular link between autophagy and apoptosis, has not been fully understood yet. The dicyano compound which we used in our study caused cell death in NSCLC cell lines. When we analyzed the cells which were treated with dicyano compound by transmission electron microscope, we observed autophagosome structures. Upon this result, we investigated expression levels of autophagic proteins in the dicyano compound-treated cells by immunoblotting and observed that expression levels of autophagic proteins were increased significantly. The TUNEL assay and qRT-PCR for pro-apoptotic and anti-apoptotic gene expression, which we performed to assess apoptosis in the dicyano compound-treated cells, showed that the cell death does not occur through apoptotic pathway. We showed that the dicyano compound, which was developed in our laboratories, may play a role in molecular link between apoptosis and autophagy and may shed light on development of new anticancer treatment strategies.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31247220</PMID><DateCompleted><Year>2019</Year><Month>08</Month><Day>15</Day></DateCompleted><DateRevised><Year>2019</Year><Month>08</Month><Day>15</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1879-0038</ISSN><JournalIssue CitedMedium="Internet"><Volume>712</Volume><PubDate><Year>2019</Year><Month>Sep</Month><Day>05</Day></PubDate></JournalIssue><Title>Gene</Title><ISOAbbreviation>Gene</ISOAbbreviation></Journal><ArticleTitle>The triazole linked galactose substituted dicyano compound can induce autophagy in NSCLC cell lines.</ArticleTitle><Pagination><MedlinePgn>143935</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0378-1119(19)30585-2</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.gene.2019.06.025</ELocationID><Abstract><AbstractText>As seen in other types of cancer, development of drug resistance in NSCLC treatment causes adverse effects on disease fighting process. Recent studies have shown that one of the drug resistance development mechanisms is that cancer cells may acquire the ability to escape from cell death. Therefore, development of anticancer drugs which have the strategy to redirect cancer cells to any cell death pathways may provide positive results for cancer treatments. Autophagy may be a target mechanism of alternative cancer treatment strategy in cases of blocked apoptosis. There is also a complex molecular link between autophagy and apoptosis, has not been fully understood yet. The dicyano compound which we used in our study caused cell death in NSCLC cell lines. When we analyzed the cells which were treated with dicyano compound by transmission electron microscope, we observed autophagosome structures. Upon this result, we investigated expression levels of autophagic proteins in the dicyano compound-treated cells by immunoblotting and observed that expression levels of autophagic proteins were increased significantly. The TUNEL assay and qRT-PCR for pro-apoptotic and anti-apoptotic gene expression, which we performed to assess apoptosis in the dicyano compound-treated cells, showed that the cell death does not occur through apoptotic pathway. We showed that the dicyano compound, which was developed in our laboratories, may play a role in molecular link between apoptosis and autophagy and may shed light on development of new anticancer treatment strategies.</AbstractText><CopyrightInformation>Copyright © 2019 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Alvur</LastName><ForeName>Ozge</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>Department of Medical Biology, Pamukkale University, Denizli, Turkey; Department of Medical Biology, Van Yuzuncu Yil University, Van, Turkey.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tokgun</LastName><ForeName>Onur</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>Department of Medical Genetics, Pamukkale University, Denizli, Turkey.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Baygu</LastName><ForeName>Yasemin</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Chemistry, Pamukkale University, Denizli, Turkey.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kabay</LastName><ForeName>Nilgun</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Biomedical Engineering, Pamukkale University, Denizli, Turkey.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gok</LastName><ForeName>Yasar</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Chemical Engineering, Usak University, Usak, Turkey.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Akca</LastName><ForeName>Hakan</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Medical Genetics, Pamukkale University, Denizli, Turkey. 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