Thymoquinone Enhances Paclitaxel Anti-Breast Cancer Activity via Inhibiting Tumor-Associated Stem Cells Despite Apparent Mathematical Antagonism
Identifieur interne : 000017 ( an2020/Analysis ); précédent : 000016; suivant : 000018Thymoquinone Enhances Paclitaxel Anti-Breast Cancer Activity via Inhibiting Tumor-Associated Stem Cells Despite Apparent Mathematical Antagonism
Auteurs : Hanan A. Bashmail ; Aliaa A. Alamoudi ; Abdulwahab Noorwali ; Gehan A. Hegazy [Égypte] ; Ghada M. Ajabnoor ; Ahmed M. Al-Abd [Égypte]Source :
- Molecules [ 1420-3049 ] ; 2020.
Abstract
Thymoquinone (TQ) has shown substantial evidence for its anticancer effects. Using human breast cancer cells, we evaluated the chemomodulatory effect of TQ on paclitaxel (PTX). TQ showed weak cytotoxic properties against MCF-7 and T47D breast cancer cells with IC50 values of 64.93 ± 14 µM and 165 ± 2 µM, respectively. Combining TQ with PTX showed apparent antagonism, increasing the IC50 values of PTX from 0.2 ± 0.07 µM to 0.7 ± 0.01 µM and from 0.1 ± 0.01 µM to 0.15 ± 0.02 µM in MCF-7 and T47D cells, respectively. Combination index analysis showed antagonism in both cell lines with CI values of 4.6 and 1.6, respectively. However, resistance fractions to PTX within MCF-7 and T47D cells (42.3 ± 1.4% and 41.9 ± 1.1%, respectively) were completely depleted by combination with TQ. TQ minimally affected the cell cycle, with moderate accumulation of cells in the S-phase. However, a significant increase in Pre-G phase cells was observed due to PTX alone and PTX combination with TQ. To dissect this increase in the Pre-G phase, apoptosis, necrosis, and autophagy were assessed by flowcytometry. TQ significantly increased the percent of apoptotic/necrotic cell death in T47D cells after combination with paclitaxel. On the other hand, TQ significantly induced autophagy in MCF-7 cells. Furthermore, TQ was found to significantly decrease breast cancer-associated stem cell clone (CD44+/CD24-cell) in both MCF-7 and T47D cells. This was mirrored by the downregulation of TWIST-1 gene and overexpression of SNAIL-1 and SNAIL-2 genes. TQ therefore possesses potential chemomodulatory effects to PTX when studied in breast cancer cells via enhancing PTX induced cell death including autophagy. In addition, TQ depletes breast cancer-associated stem cells and sensitizes breast cancer cells to PTX killing effects.
Url:
DOI: 10.3390/molecules25020426
PubMed: 31968657
PubMed Central: 7024316
Affiliations:
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Alamoudi</name><affiliation><nlm:aff id="af1-molecules-25-00426">Department of Clinical Biochemistry, Faculty of Medicine, King Abdulaziz University, Jeddah 21589, Saudi Arabia;<email>hanan.a.bashmail@gmail.com</email> (H.A.B.);<email>aliaa.alamo@gmail.com</email> (A.A.A.);<email>wal5566@gmail.com</email> (A.N.);<email>gehanhegazy@hotmail.com</email> (G.A.H.);<email>ga_clinbio@yahoo.com</email> (G.M.A.)</nlm:aff></affiliation></author><author><name sortKey="Noorwali, Abdulwahab" sort="Noorwali, Abdulwahab" uniqKey="Noorwali A" first="Abdulwahab" last="Noorwali">Abdulwahab Noorwali</name><affiliation><nlm:aff id="af1-molecules-25-00426">Department of Clinical Biochemistry, Faculty of Medicine, King Abdulaziz University, Jeddah 21589, Saudi Arabia;<email>hanan.a.bashmail@gmail.com</email> (H.A.B.);<email>aliaa.alamo@gmail.com</email> (A.A.A.);<email>wal5566@gmail.com</email> (A.N.);<email>gehanhegazy@hotmail.com</email> (G.A.H.);<email>ga_clinbio@yahoo.com</email> (G.M.A.)</nlm:aff></affiliation></author><author><name sortKey="Hegazy, Gehan A" sort="Hegazy, Gehan A" uniqKey="Hegazy G" first="Gehan A." last="Hegazy">Gehan A. 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Ajabnoor</name><affiliation><nlm:aff id="af1-molecules-25-00426">Department of Clinical Biochemistry, Faculty of Medicine, King Abdulaziz University, Jeddah 21589, Saudi Arabia;<email>hanan.a.bashmail@gmail.com</email> (H.A.B.);<email>aliaa.alamo@gmail.com</email> (A.A.A.);<email>wal5566@gmail.com</email> (A.N.);<email>gehanhegazy@hotmail.com</email> (G.A.H.);<email>ga_clinbio@yahoo.com</email> (G.M.A.)</nlm:aff></affiliation></author><author><name sortKey="Al Abd, Ahmed M" sort="Al Abd, Ahmed M" uniqKey="Al Abd A" first="Ahmed M." last="Al-Abd">Ahmed M. 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Bashmail</name><affiliation><nlm:aff id="af1-molecules-25-00426">Department of Clinical Biochemistry, Faculty of Medicine, King Abdulaziz University, Jeddah 21589, Saudi Arabia;<email>hanan.a.bashmail@gmail.com</email> (H.A.B.);<email>aliaa.alamo@gmail.com</email> (A.A.A.);<email>wal5566@gmail.com</email> (A.N.);<email>gehanhegazy@hotmail.com</email> (G.A.H.);<email>ga_clinbio@yahoo.com</email> (G.M.A.)</nlm:aff></affiliation></author><author><name sortKey="Alamoudi, Aliaa A" sort="Alamoudi, Aliaa A" uniqKey="Alamoudi A" first="Aliaa A." last="Alamoudi">Aliaa A. Alamoudi</name><affiliation><nlm:aff id="af1-molecules-25-00426">Department of Clinical Biochemistry, Faculty of Medicine, King Abdulaziz University, Jeddah 21589, Saudi Arabia;<email>hanan.a.bashmail@gmail.com</email> (H.A.B.);<email>aliaa.alamo@gmail.com</email> (A.A.A.);<email>wal5566@gmail.com</email> (A.N.);<email>gehanhegazy@hotmail.com</email> (G.A.H.);<email>ga_clinbio@yahoo.com</email> (G.M.A.)</nlm:aff></affiliation></author><author><name sortKey="Noorwali, Abdulwahab" sort="Noorwali, Abdulwahab" uniqKey="Noorwali A" first="Abdulwahab" last="Noorwali">Abdulwahab Noorwali</name><affiliation><nlm:aff id="af1-molecules-25-00426">Department of Clinical Biochemistry, Faculty of Medicine, King Abdulaziz University, Jeddah 21589, Saudi Arabia;<email>hanan.a.bashmail@gmail.com</email> (H.A.B.);<email>aliaa.alamo@gmail.com</email> (A.A.A.);<email>wal5566@gmail.com</email> (A.N.);<email>gehanhegazy@hotmail.com</email> (G.A.H.);<email>ga_clinbio@yahoo.com</email> (G.M.A.)</nlm:aff></affiliation></author><author><name sortKey="Hegazy, Gehan A" sort="Hegazy, Gehan A" uniqKey="Hegazy G" first="Gehan A." last="Hegazy">Gehan A. Hegazy</name><affiliation><nlm:aff id="af1-molecules-25-00426">Department of Clinical Biochemistry, Faculty of Medicine, King Abdulaziz University, Jeddah 21589, Saudi Arabia;<email>hanan.a.bashmail@gmail.com</email> (H.A.B.);<email>aliaa.alamo@gmail.com</email> (A.A.A.);<email>wal5566@gmail.com</email> (A.N.);<email>gehanhegazy@hotmail.com</email> (G.A.H.);<email>ga_clinbio@yahoo.com</email> (G.M.A.)</nlm:aff></affiliation><affiliation wicri:level="1"><nlm:aff id="af2-molecules-25-00426">Department of Medical Biochemistry, Medical Division, National Research Centre, Giza 12622, Egypt</nlm:aff><country xml:lang="fr">Égypte</country><wicri:regionArea>Department of Medical Biochemistry, Medical Division, National Research Centre, Giza 12622</wicri:regionArea><wicri:noRegion>Giza 12622</wicri:noRegion></affiliation></author><author><name sortKey="Ajabnoor, Ghada M" sort="Ajabnoor, Ghada M" uniqKey="Ajabnoor G" first="Ghada M." last="Ajabnoor">Ghada M. Ajabnoor</name><affiliation><nlm:aff id="af1-molecules-25-00426">Department of Clinical Biochemistry, Faculty of Medicine, King Abdulaziz University, Jeddah 21589, Saudi Arabia;<email>hanan.a.bashmail@gmail.com</email> (H.A.B.);<email>aliaa.alamo@gmail.com</email> (A.A.A.);<email>wal5566@gmail.com</email> (A.N.);<email>gehanhegazy@hotmail.com</email> (G.A.H.);<email>ga_clinbio@yahoo.com</email> (G.M.A.)</nlm:aff></affiliation></author><author><name sortKey="Al Abd, Ahmed M" sort="Al Abd, Ahmed M" uniqKey="Al Abd A" first="Ahmed M." last="Al-Abd">Ahmed M. Al-Abd</name><affiliation><nlm:aff id="af3-molecules-25-00426">Department of Pharmaceutical Sciences, College of Pharmacy, Gulf Medical University, Ajman 4184, UAE</nlm:aff><wicri:noCountry code="subfield">UAE</wicri:noCountry></affiliation><affiliation wicri:level="1"><nlm:aff id="af4-molecules-25-00426">Department of Pharmacology, Medical Division, National Research Centre, Giza 12622, Egypt</nlm:aff><country xml:lang="fr">Égypte</country><wicri:regionArea>Department of Pharmacology, Medical Division, National Research Centre, Giza 12622</wicri:regionArea><wicri:noRegion>Giza 12622</wicri:noRegion></affiliation></author></analytic><series><title level="j">Molecules</title><idno type="eISSN">1420-3049</idno><imprint><date when="2020">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Thymoquinone (TQ) has shown substantial evidence for its anticancer effects. Using human breast cancer cells, we evaluated the chemomodulatory effect of TQ on paclitaxel (PTX). TQ showed weak cytotoxic properties against MCF-7 and T47D breast cancer cells with IC<sub>50</sub> values of 64.93 ± 14 µM and 165 ± 2 µM, respectively. Combining TQ with PTX showed apparent antagonism, increasing the IC<sub>50</sub> values of PTX from 0.2 ± 0.07 µM to 0.7 ± 0.01 µM and from 0.1 ± 0.01 µM to 0.15 ± 0.02 µM in MCF-7 and T47D cells, respectively. Combination index analysis showed antagonism in both cell lines with CI values of 4.6 and 1.6, respectively. However, resistance fractions to PTX within MCF-7 and T47D cells (42.3 ± 1.4% and 41.9 ± 1.1%, respectively) were completely depleted by combination with TQ. TQ minimally affected the cell cycle, with moderate accumulation of cells in the S-phase. However, a significant increase in Pre-G phase cells was observed due to PTX alone and PTX combination with TQ. To dissect this increase in the Pre-G phase, apoptosis, necrosis, and autophagy were assessed by flowcytometry. TQ significantly increased the percent of apoptotic/necrotic cell death in T47D cells after combination with paclitaxel. On the other hand, TQ significantly induced autophagy in MCF-7 cells. Furthermore, TQ was found to significantly decrease breast cancer-associated stem cell clone (CD44+/CD24-cell) in both MCF-7 and T47D cells. This was mirrored by the downregulation of TWIST-1 gene and overexpression of SNAIL-1 and SNAIL-2 genes. TQ therefore possesses potential chemomodulatory effects to PTX when studied in breast cancer cells via enhancing PTX induced cell death including autophagy. In addition, TQ depletes breast cancer-associated stem cells and sensitizes breast cancer cells to PTX killing effects.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Clardy, J" uniqKey="Clardy J">J. 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Ajabnoor</name><name sortKey="Alamoudi, Aliaa A" sort="Alamoudi, Aliaa A" uniqKey="Alamoudi A" first="Aliaa A." last="Alamoudi">Aliaa A. Alamoudi</name><name sortKey="Bashmail, Hanan A" sort="Bashmail, Hanan A" uniqKey="Bashmail H" first="Hanan A." last="Bashmail">Hanan A. Bashmail</name><name sortKey="Noorwali, Abdulwahab" sort="Noorwali, Abdulwahab" uniqKey="Noorwali A" first="Abdulwahab" last="Noorwali">Abdulwahab Noorwali</name></noCountry><country name="Égypte"><noRegion><name sortKey="Hegazy, Gehan A" sort="Hegazy, Gehan A" uniqKey="Hegazy G" first="Gehan A." last="Hegazy">Gehan A. Hegazy</name></noRegion><name sortKey="Al Abd, Ahmed M" sort="Al Abd, Ahmed M" uniqKey="Al Abd A" first="Ahmed M." last="Al-Abd">Ahmed M. Al-Abd</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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