Autophagy inhibition enhances Matrine derivative MASM induced apoptosis in cancer cells via a mechanism involving reactive oxygen species-mediated PI3K/Akt/mTOR and Erk/p38 signaling
Identifieur interne : 000A29 ( Main/Exploration ); précédent : 000A28; suivant : 000A30Autophagy inhibition enhances Matrine derivative MASM induced apoptosis in cancer cells via a mechanism involving reactive oxygen species-mediated PI3K/Akt/mTOR and Erk/p38 signaling
Auteurs : Yuming Zou [Allemagne, République populaire de Chine] ; Melika Sarem [Allemagne] ; Shengnan Xiang [Allemagne] ; Honggang Hu [République populaire de Chine] ; Weidong Xu [République populaire de Chine] ; V. Prasad Shastri [Allemagne]Source :
- BMC Cancer [ 1471-2407 ] ; 2019.
Abstract
In the quest for new anti-cancer drugs, the drug discovery process has shifted to screening of active ingredients in traditional eastern medicine. Matrine is an active alkaloid isolated from plants of the Sophora genus used in traditional Chinese herbal medicine that exhibits a wide spectrum of biological properties and has a potential as an anti-proliferative agent. In this study, we investigated the anticancer property of MASM, ([(6aS, 10S, 11aR, 11bR, 11cS)210-Methylamino-dodecahydro-3a, 7a-diaza-benzo (de)anthracene-8-thione]), a potent derivative of matrine.
Four epithelial cancer cell lines representing the dominant cancers, namely: A549 (non-small-cell lung cancer cell line), MCF-7 and MDA-MB-231 (breast cancer cell lines), and Hela (cervical cancer cell line) were employed, and the mechanistic underpinning of MASM-induced apoptosis was investigated using flow cytometry, western blot and immunofluorescence.
MASM, induced apoptosis via caspase 3 dependent and independent pathways, and autophagy in all the four cancer cell lines, but post-EMT (epithelial mesenchymal transition) cells showed greater sensitivity to MASM. Scavenging reactive oxygen species using N-acetylcysteine rescued all cancer cell lines from apoptosis and autophagy. Mechanistic analysis revealed that MASM induced autophagy involves inhibition of Akt signaling and the activation of Erk and p38 signaling, and inhibition of autophagy further enhanced the apoptosis induced by MASM.
These results indicate that MASM possesses potency against cancer cells and modulating autophagy during MASM administration could be used to further enhance its therapeutic effects.
Url:
DOI: 10.1186/s12885-019-6199-7
PubMed: 31615459
PubMed Central: 6794878
Affiliations:
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type="main">Autophagy inhibition enhances Matrine derivative MASM induced apoptosis in cancer cells via a mechanism involving reactive oxygen species-mediated PI3K/Akt/mTOR and Erk/p38 signaling</title><author><name sortKey="Zou, Yuming" sort="Zou, Yuming" uniqKey="Zou Y" first="Yuming" last="Zou">Yuming Zou</name><affiliation wicri:level="1"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.5963.9</institution-id><institution>Institute for Macromolecular Chemistry,</institution><institution>University of Freiburg,</institution></institution-wrap>79104 Freiburg, Germany</nlm:aff><country xml:lang="fr">Allemagne</country><wicri:regionArea>79104 Freiburg</wicri:regionArea></affiliation><affiliation><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1758 2270</institution-id><institution-id institution-id-type="GRID">grid.412632.0</institution-id><institution>Department of Orthopaedics, Department of Orthopaedics,</institution><institution>People’s Hospital of Wuhan University,</institution></institution-wrap>Wuhan, 430060 Hubei Province People’s Republic of China</nlm:aff><wicri:noCountry code="subfield">430060 Hubei Province People’s Republic of China</wicri:noCountry></affiliation><affiliation wicri:level="1"><nlm:aff id="Aff3"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 0369 1660</institution-id><institution-id institution-id-type="GRID">grid.73113.37</institution-id><institution>Department of Orthopaedics, Changhai hospital,</institution><institution>Second Military Medical University,</institution></institution-wrap>Shanghai, 200433 People’s Republic of China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Shanghai</wicri:regionArea></affiliation><affiliation><nlm:aff id="Aff4"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2267 2324</institution-id><institution-id institution-id-type="GRID">grid.488137.1</institution-id><institution>Department of Orthopaedics, the 904th Hospital of Joint Logistic Support Force, Chinese People’s Liberation Army,</institution></institution-wrap>Wuxi, Jiangsu Province People’s Republic of China</nlm:aff><wicri:noCountry code="subfield">Jiangsu Province People’s Republic of China</wicri:noCountry></affiliation></author><author><name sortKey="Sarem, Melika" sort="Sarem, Melika" uniqKey="Sarem M" first="Melika" last="Sarem">Melika Sarem</name><affiliation wicri:level="1"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.5963.9</institution-id><institution>Institute for Macromolecular Chemistry,</institution><institution>University of Freiburg,</institution></institution-wrap>79104 Freiburg, Germany</nlm:aff><country xml:lang="fr">Allemagne</country><wicri:regionArea>79104 Freiburg</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="Aff5"><institution-wrap><institution-id institution-id-type="GRID">grid.5963.9</institution-id><institution>BIOSS Centre for Biological Signalling Studies,</institution><institution>University of Freiburg,</institution></institution-wrap>79104 Freiburg, Germany</nlm:aff><country xml:lang="fr">Allemagne</country><wicri:regionArea>79104 Freiburg</wicri:regionArea></affiliation></author><author><name sortKey="Xiang, Shengnan" sort="Xiang, Shengnan" uniqKey="Xiang S" first="Shengnan" last="Xiang">Shengnan Xiang</name><affiliation wicri:level="1"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.5963.9</institution-id><institution>Institute for Macromolecular Chemistry,</institution><institution>University of Freiburg,</institution></institution-wrap>79104 Freiburg, Germany</nlm:aff><country xml:lang="fr">Allemagne</country><wicri:regionArea>79104 Freiburg</wicri:regionArea></affiliation></author><author><name sortKey="Hu, Honggang" sort="Hu, Honggang" uniqKey="Hu H" first="Honggang" last="Hu">Honggang Hu</name><affiliation wicri:level="1"><nlm:aff id="Aff6"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 0369 1660</institution-id><institution-id institution-id-type="GRID">grid.73113.37</institution-id><institution>Department of Organic Chemistry, School of Pharmacy,</institution><institution>Second Military Medical University,</institution></institution-wrap>Shanghai, 200433 People’s Republic of China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Shanghai</wicri:regionArea></affiliation></author><author><name sortKey="Xu, Weidong" sort="Xu, Weidong" uniqKey="Xu W" first="Weidong" last="Xu">Weidong Xu</name><affiliation wicri:level="1"><nlm:aff id="Aff3"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 0369 1660</institution-id><institution-id institution-id-type="GRID">grid.73113.37</institution-id><institution>Department of Orthopaedics, Changhai hospital,</institution><institution>Second Military Medical University,</institution></institution-wrap>Shanghai, 200433 People’s Republic of China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Shanghai</wicri:regionArea></affiliation></author><author><name sortKey="Shastri, V Prasad" sort="Shastri, V Prasad" uniqKey="Shastri V" first="V. Prasad" last="Shastri">V. Prasad Shastri</name><affiliation wicri:level="1"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.5963.9</institution-id><institution>Institute for Macromolecular Chemistry,</institution><institution>University of Freiburg,</institution></institution-wrap>79104 Freiburg, Germany</nlm:aff><country xml:lang="fr">Allemagne</country><wicri:regionArea>79104 Freiburg</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="Aff5"><institution-wrap><institution-id institution-id-type="GRID">grid.5963.9</institution-id><institution>BIOSS Centre for Biological Signalling Studies,</institution><institution>University of Freiburg,</institution></institution-wrap>79104 Freiburg, Germany</nlm:aff><country xml:lang="fr">Allemagne</country><wicri:regionArea>79104 Freiburg</wicri:regionArea></affiliation></author></analytic><series><title level="j">BMC Cancer</title><idno type="eISSN">1471-2407</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec><title>Background</title><p id="Par1">In the quest for new anti-cancer drugs, the drug discovery process has shifted to screening of active ingredients in traditional eastern medicine. Matrine is an active alkaloid isolated from plants of the Sophora genus used in traditional Chinese herbal medicine that exhibits a wide spectrum of biological properties and has a potential as an anti-proliferative agent. In this study, we investigated the anticancer property of MASM, ([(6aS, 10S, 11aR, 11bR, 11cS)210-Methylamino-dodecahydro-3a, 7a-diaza-benzo (de)anthracene-8-thione]), a potent derivative of matrine.</p></sec><sec><title>Methods</title><p id="Par2">Four epithelial cancer cell lines representing the dominant cancers, namely: A549 (non-small-cell lung cancer cell line), MCF-7 and MDA-MB-231 (breast cancer cell lines), and Hela (cervical cancer cell line) were employed, and the mechanistic underpinning of MASM-induced apoptosis was investigated using flow cytometry, western blot and immunofluorescence.</p></sec><sec><title>Results</title><p id="Par3">MASM, induced apoptosis via caspase 3 dependent and independent pathways, and autophagy in all the four cancer cell lines, but post-EMT (epithelial mesenchymal transition) cells showed greater sensitivity to MASM. Scavenging reactive oxygen species using N-acetylcysteine rescued all cancer cell lines from apoptosis and autophagy. Mechanistic analysis revealed that MASM induced autophagy involves inhibition of Akt signaling and the activation of Erk and p38 signaling, and inhibition of autophagy further enhanced the apoptosis induced by MASM.</p></sec><sec><title>Conclusions</title><p id="Par4">These results indicate that MASM possesses potency against cancer cells and modulating autophagy during MASM administration could be used to further enhance its therapeutic effects.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Fitzmaurice, C" uniqKey="Fitzmaurice C">C Fitzmaurice</name></author><author><name sortKey="Allen, C" uniqKey="Allen C">C Allen</name></author><author><name sortKey="Barber, Rm" uniqKey="Barber R">RM Barber</name></author><author><name sortKey="Barregard, L" uniqKey="Barregard L">L Barregard</name></author><author><name sortKey="Bhutta, Za" uniqKey="Bhutta Z">ZA 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Shao</name></author><author><name sortKey="Yang, B" uniqKey="Yang B">B Yang</name></author><author><name sortKey="Hu, R" uniqKey="Hu R">R Hu</name></author><author><name sortKey="Wang, Y" uniqKey="Wang Y">Y Wang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liu, Yq" uniqKey="Liu Y">YQ Liu</name></author><author><name sortKey="Li, Y" uniqKey="Li Y">Y Li</name></author><author><name sortKey="Qin, J" uniqKey="Qin J">J Qin</name></author><author><name sortKey="Wang, Q" uniqKey="Wang Q">Q Wang</name></author><author><name sortKey="She, Yl" uniqKey="She Y">YL She</name></author><author><name sortKey="Luo, Yl" uniqKey="Luo Y">YL Luo</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Gibson, Sb" uniqKey="Gibson S">SB Gibson</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Allemagne</li><li>République populaire de Chine</li></country></list><tree><country name="Allemagne"><noRegion><name sortKey="Zou, Yuming" sort="Zou, Yuming" uniqKey="Zou Y" first="Yuming" last="Zou">Yuming Zou</name></noRegion><name sortKey="Sarem, Melika" sort="Sarem, Melika" uniqKey="Sarem M" first="Melika" last="Sarem">Melika Sarem</name><name sortKey="Sarem, Melika" sort="Sarem, Melika" uniqKey="Sarem M" first="Melika" last="Sarem">Melika Sarem</name><name sortKey="Shastri, V Prasad" sort="Shastri, V Prasad" uniqKey="Shastri V" first="V. Prasad" last="Shastri">V. Prasad Shastri</name><name sortKey="Shastri, V Prasad" sort="Shastri, V Prasad" uniqKey="Shastri V" first="V. Prasad" last="Shastri">V. Prasad Shastri</name><name sortKey="Xiang, Shengnan" sort="Xiang, Shengnan" uniqKey="Xiang S" first="Shengnan" last="Xiang">Shengnan Xiang</name></country><country name="République populaire de Chine"><noRegion><name sortKey="Zou, Yuming" sort="Zou, Yuming" uniqKey="Zou Y" first="Yuming" last="Zou">Yuming Zou</name></noRegion><name sortKey="Hu, Honggang" sort="Hu, Honggang" uniqKey="Hu H" first="Honggang" last="Hu">Honggang Hu</name><name sortKey="Xu, Weidong" sort="Xu, Weidong" uniqKey="Xu W" first="Weidong" last="Xu">Weidong Xu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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