Autophagy inhibition with chloroquine reverts paclitaxel resistance and attenuates metastatic potential in human nonsmall lung adenocarcinoma A549 cells via ROS mediated modulation of β-catenin pathway.
Identifieur interne : 000A25 ( Main/Exploration ); précédent : 000A24; suivant : 000A26Autophagy inhibition with chloroquine reverts paclitaxel resistance and attenuates metastatic potential in human nonsmall lung adenocarcinoma A549 cells via ROS mediated modulation of β-catenin pathway.
Auteurs : Satabdi Datta [Inde] ; Diptiman Choudhury [Inde] ; Amlan Das [Inde] ; Dipanwita Das Mukherjee [Inde] ; Moumita Dasgupta [Inde] ; Shreya Bandopadhyay [Inde] ; Gopal Chakrabarti [Inde]Source :
- Apoptosis : an international journal on programmed cell death [ 1573-675X ] ; 2019.
Abstract
Paclitaxel is one of the most commonly used drugs for the treatment of nonsmall cell lung cancer (NSCLC). However acquired resistance to paclitaxel, epithelial to mesenchymal transition and cancer stem cell formation are the major obstacles for successful chemotherapy with this drug. Some of the major reasons behind chemoresistance development include increased ability of the cancer cells to survive under stress conditions by autophagy, increased expression of drug efflux pumps, tubulin mutations etc. In this study we found that inhibition of autophagy with chloroquine prevented development of paclitaxel resistance in A549 cells with time and potentiated the effect of paclitaxel by increased accumulation of superoxide-producing damaged mitochondria, with elevated ROS generation, it also increased the apoptotic rate and sub G0/ G1 phase arrest with time in A549 cells treated with paclitaxel and attenuated the metastatic potential and cancer stem cell population of the paclitaxel-resistant cells by ROS mediated modulation of the Wnt/β-catenin signaling pathway, thereby increasing paclitaxel sensitivity. ROS here played a crucial role in modulating Akt activity when autophagy process was hindered by chloroquine, excessive ROS accumulation in the cell inhibited Akt activity. In addition, chloroquine pre-treatment followed by taxol (10 nM) treatment did not show significant toxicity towards non-carcinomas WI38 cells (lung fibroblast cells). Thus autophagy inhibition by CQ pre-treatment can be used as a fruitful strategy to combat the phenomenon of paclitaxel resistance development as well as metastasis in lung cancer.
DOI: 10.1007/s10495-019-01526-y
PubMed: 30767087
Affiliations:
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Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Ballygunge, Kolkata, West Bengal, 700 019</wicri:regionArea><wicri:noRegion>700 019</wicri:noRegion></affiliation></author><author><name sortKey="Choudhury, Diptiman" sort="Choudhury, Diptiman" uniqKey="Choudhury D" first="Diptiman" last="Choudhury">Diptiman Choudhury</name><affiliation wicri:level="1"><nlm:affiliation>School of Chemistry and Biochemistry, Thapar Institute of Engineering and Technology, Bhadson Road, Patiala, Punjab, 147004, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>School of Chemistry and Biochemistry, Thapar Institute of Engineering and Technology, Bhadson Road, Patiala, Punjab, 147004</wicri:regionArea><wicri:noRegion>147004</wicri:noRegion></affiliation></author><author><name sortKey="Das, Amlan" sort="Das, Amlan" uniqKey="Das A" first="Amlan" last="Das">Amlan Das</name><affiliation wicri:level="1"><nlm:affiliation>Department of Chemistry, National Institute of Technology, Ravangla, Sikkim, 737139, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Department of Chemistry, National Institute of Technology, Ravangla, Sikkim, 737139</wicri:regionArea><wicri:noRegion>737139</wicri:noRegion></affiliation></author><author><name sortKey="Mukherjee, Dipanwita Das" sort="Mukherjee, Dipanwita Das" uniqKey="Mukherjee D" first="Dipanwita Das" last="Mukherjee">Dipanwita Das Mukherjee</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biotechnology and Dr. B. 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Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Ballygunge, Kolkata, West Bengal, 700 019</wicri:regionArea><wicri:noRegion>700 019</wicri:noRegion></affiliation></author><author><name sortKey="Bandopadhyay, Shreya" sort="Bandopadhyay, Shreya" uniqKey="Bandopadhyay S" first="Shreya" last="Bandopadhyay">Shreya Bandopadhyay</name><affiliation wicri:level="1"><nlm:affiliation>Cell Biology & Physiology Division, CSIR - Indian Institute of Chemical Biology, Kolkata, 700032, India.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Cell Biology & Physiology Division, CSIR - Indian Institute of Chemical Biology, Kolkata, 700032</wicri:regionArea><wicri:noRegion>700032</wicri:noRegion></affiliation></author><author><name sortKey="Chakrabarti, Gopal" sort="Chakrabarti, Gopal" uniqKey="Chakrabarti G" first="Gopal" last="Chakrabarti">Gopal Chakrabarti</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biotechnology and Dr. B. C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Ballygunge, Kolkata, West Bengal, 700 019, India. gcbcg@caluniv.ac.in.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Department of Biotechnology and Dr. B. C. Guha Centre for Genetic Engineering and Biotechnology, University of Calcutta, 35 Ballygunge Circular Road, Ballygunge, Kolkata, West Bengal, 700 019</wicri:regionArea><wicri:noRegion>700 019</wicri:noRegion></affiliation></author></analytic><series><title level="j">Apoptosis : an international journal on programmed cell death</title><idno type="eISSN">1573-675X</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Paclitaxel is one of the most commonly used drugs for the treatment of nonsmall cell lung cancer (NSCLC). However acquired resistance to paclitaxel, epithelial to mesenchymal transition and cancer stem cell formation are the major obstacles for successful chemotherapy with this drug. Some of the major reasons behind chemoresistance development include increased ability of the cancer cells to survive under stress conditions by autophagy, increased expression of drug efflux pumps, tubulin mutations etc. In this study we found that inhibition of autophagy with chloroquine prevented development of paclitaxel resistance in A549 cells with time and potentiated the effect of paclitaxel by increased accumulation of superoxide-producing damaged mitochondria, with elevated ROS generation, it also increased the apoptotic rate and sub G0/ G1 phase arrest with time in A549 cells treated with paclitaxel and attenuated the metastatic potential and cancer stem cell population of the paclitaxel-resistant cells by ROS mediated modulation of the Wnt/β-catenin signaling pathway, thereby increasing paclitaxel sensitivity. ROS here played a crucial role in modulating Akt activity when autophagy process was hindered by chloroquine, excessive ROS accumulation in the cell inhibited Akt activity. In addition, chloroquine pre-treatment followed by taxol (10 nM) treatment did not show significant toxicity towards non-carcinomas WI38 cells (lung fibroblast cells). Thus autophagy inhibition by CQ pre-treatment can be used as a fruitful strategy to combat the phenomenon of paclitaxel resistance development as well as metastasis in lung cancer.</div></front></TEI><affiliations><list><country><li>Inde</li></country></list><tree><country name="Inde"><noRegion><name sortKey="Datta, Satabdi" sort="Datta, Satabdi" uniqKey="Datta S" first="Satabdi" last="Datta">Satabdi Datta</name></noRegion><name sortKey="Bandopadhyay, Shreya" sort="Bandopadhyay, Shreya" uniqKey="Bandopadhyay S" first="Shreya" last="Bandopadhyay">Shreya Bandopadhyay</name><name sortKey="Chakrabarti, Gopal" sort="Chakrabarti, Gopal" uniqKey="Chakrabarti G" first="Gopal" last="Chakrabarti">Gopal Chakrabarti</name><name sortKey="Choudhury, Diptiman" sort="Choudhury, Diptiman" uniqKey="Choudhury D" first="Diptiman" last="Choudhury">Diptiman Choudhury</name><name sortKey="Das, Amlan" sort="Das, Amlan" uniqKey="Das A" first="Amlan" last="Das">Amlan Das</name><name sortKey="Dasgupta, Moumita" sort="Dasgupta, Moumita" uniqKey="Dasgupta M" first="Moumita" last="Dasgupta">Moumita Dasgupta</name><name sortKey="Mukherjee, Dipanwita Das" sort="Mukherjee, Dipanwita Das" uniqKey="Mukherjee D" first="Dipanwita Das" last="Mukherjee">Dipanwita Das Mukherjee</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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