The triazole linked galactose substituted dicyano compound can induce autophagy in NSCLC cell lines.
Identifieur interne : 000332 ( Main/Exploration ); précédent : 000331; suivant : 000333The triazole linked galactose substituted dicyano compound can induce autophagy in NSCLC cell lines.
Auteurs : Ozge Alvur [Turquie] ; Onur Tokgun [Turquie] ; Yasemin Baygu [Turquie] ; Nilgun Kabay [Turquie] ; Yasar Gok [Turquie] ; Hakan Akca [Turquie]Source :
- Gene [ 1879-0038 ] ; 2019.
Descripteurs français
- KwdFr :
- Antinéoplasiques, Apoptose, Autophagie, Carcinome pulmonaire non à petites cellules (métabolisme), Carcinome pulmonaire non à petites cellules (traitement médicamenteux), Chloroquine (), Concentration inhibitrice 50, Galactose (), Humains, Lignée cellulaire tumorale, Microscopie électronique à transmission, Naphtyridines (métabolisme), Prolifération cellulaire (), Protéines adaptatrices de la transduction du signal (métabolisme), Protéines associées aux microtubules (métabolisme), Protéines régulatrices de l'apoptose (métabolisme), Résistance aux médicaments antinéoplasiques, Survie cellulaire (), Sérine-thréonine kinases TOR (métabolisme), Tests de criblage d'agents antitumoraux, Transduction du signal (), Triazoles (), Tumeurs du poumon (métabolisme), Tumeurs du poumon (traitement médicamenteux).
- MESH :
- métabolisme : Carcinome pulmonaire non à petites cellules, Naphtyridines, Protéines adaptatrices de la transduction du signal, Protéines associées aux microtubules, Protéines régulatrices de l'apoptose, Sérine-thréonine kinases TOR, Tumeurs du poumon.
- traitement médicamenteux : Carcinome pulmonaire non à petites cellules, Tumeurs du poumon.
- Antinéoplasiques, Apoptose, Autophagie, Chloroquine, Concentration inhibitrice 50, Galactose, Humains, Lignée cellulaire tumorale, Microscopie électronique à transmission, Prolifération cellulaire, Résistance aux médicaments antinéoplasiques, Survie cellulaire, Tests de criblage d'agents antitumoraux, Transduction du signal, Triazoles.
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
Affiliations:
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Electronic address: hakca@pau.edu.tr.</nlm:affiliation><country xml:lang="fr">Turquie</country><wicri:regionArea>Department of Medical Genetics, Pamukkale University, Denizli</wicri:regionArea><wicri:noRegion>Denizli</wicri:noRegion></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="KwdFr" xml:lang="fr"><term>Antinéoplasiques</term><term>Apoptose</term><term>Autophagie</term><term>Carcinome pulmonaire non à petites cellules (métabolisme)</term><term>Carcinome pulmonaire non à petites cellules (traitement médicamenteux)</term><term>Chloroquine ()</term><term>Concentration inhibitrice 50</term><term>Galactose ()</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Microscopie électronique à transmission</term><term>Naphtyridines (métabolisme)</term><term>Prolifération cellulaire ()</term><term>Protéines adaptatrices de la transduction du signal (métabolisme)</term><term>Protéines associées aux microtubules (métabolisme)</term><term>Protéines régulatrices de l'apoptose (métabolisme)</term><term>Résistance aux médicaments antinéoplasiques</term><term>Survie cellulaire ()</term><term>Sérine-thréonine kinases TOR (métabolisme)</term><term>Tests de criblage d'agents antitumoraux</term><term>Transduction du signal ()</term><term>Triazoles ()</term><term>Tumeurs du poumon (métabolisme)</term><term>Tumeurs du poumon (traitement médicamenteux)</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" qualifier="métabolisme" xml:lang="fr"><term>Carcinome pulmonaire non à petites cellules</term><term>Naphtyridines</term><term>Protéines adaptatrices de la transduction du signal</term><term>Protéines associées aux microtubules</term><term>Protéines régulatrices de l'apoptose</term><term>Sérine-thréonine kinases TOR</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Carcinome pulmonaire non à petites cellules</term><term>Tumeurs du poumon</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><keywords scheme="MESH" xml:lang="fr"><term>Antinéoplasiques</term><term>Apoptose</term><term>Autophagie</term><term>Chloroquine</term><term>Concentration inhibitrice 50</term><term>Galactose</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Microscopie électronique à transmission</term><term>Prolifération cellulaire</term><term>Résistance aux médicaments antinéoplasiques</term><term>Survie cellulaire</term><term>Tests de criblage d'agents antitumoraux</term><term>Transduction du signal</term><term>Triazoles</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><affiliations><list><country><li>Turquie</li></country></list><tree><country name="Turquie"><noRegion><name sortKey="Alvur, Ozge" sort="Alvur, Ozge" uniqKey="Alvur O" first="Ozge" last="Alvur">Ozge Alvur</name></noRegion><name sortKey="Akca, Hakan" sort="Akca, Hakan" uniqKey="Akca H" first="Hakan" last="Akca">Hakan Akca</name><name sortKey="Baygu, Yasemin" sort="Baygu, Yasemin" uniqKey="Baygu Y" first="Yasemin" last="Baygu">Yasemin Baygu</name><name sortKey="Gok, Yasar" sort="Gok, Yasar" uniqKey="Gok Y" first="Yasar" last="Gok">Yasar Gok</name><name sortKey="Kabay, Nilgun" sort="Kabay, Nilgun" uniqKey="Kabay N" first="Nilgun" last="Kabay">Nilgun Kabay</name><name sortKey="Tokgun, Onur" sort="Tokgun, Onur" uniqKey="Tokgun O" first="Onur" last="Tokgun">Onur Tokgun</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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