GMI, an Immunomodulatory Protein from Ganoderma microsporum, Potentiates Cisplatin-Induced Apoptosis via Autophagy in Lung Cancer Cells.
Identifieur interne : 000E87 ( Main/Exploration ); précédent : 000E86; suivant : 000E88GMI, an Immunomodulatory Protein from Ganoderma microsporum, Potentiates Cisplatin-Induced Apoptosis via Autophagy in Lung Cancer Cells.
Auteurs : I-Lun Hsin [Taïwan] ; Chu-Chyn Ou [Taïwan] ; Ming-Fang Wu [Taïwan] ; Ming-Shiou Jan [Taïwan] ; Yi-Min Hsiao [Taïwan] ; Ching-Hsiung Lin [Taïwan] ; Jiunn-Liang Ko [Taïwan]Source :
- Molecular pharmaceutics [ 1543-8392 ] ; 2015.
Descripteurs français
- KwdFr :
- MESH :
- métabolisme : Caspase-3, Caspase-7, Tumeurs du poumon.
- pharmacologie : Cisplatine, Protéines fongiques.
- Apoptose, Autophagie, Ganoderma, Humains, Lignée cellulaire, Survie cellulaire.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Caspase 3, Caspase 7.
- chemistry : Ganoderma.
- drug effects : Apoptosis, Autophagy, Cell Survival.
- metabolism : Lung Neoplasms.
- chemical , pharmacology : Cisplatin, Fungal Proteins.
- Cell Line, Humans.
Abstract
Cisplatin-based therapy is common in the treatment of several types of cancers, including lung cancers. In our previous study, GMI, an immunomodulatory protein cloned from Ganoderma microsporum, induced a cytotoxic effect in lung cancer cells via autophagy. The aim of this study is to examine the role of GMI in enhancing cisplatin-mediated cell death. On the basis of MTT assay and Combination Index, GMI and cisplatin cotreatment induced a synergistic cytotoxic effect. GMI and cisplatin-induced apoptosis was determined by sub-G1, nuclear condensation, and annexin-V/propidium iodide analyses. On Western blot, expressions of γH2AX and cleaved forms of PARP, caspase-3, and caspase-7 were induced by combined treatment. Akt/mTOR pathway activity, LC3-II expression, and acidic vesicular organelle development demonstrated that cisplatin does not abolish GMI-mediated autophagy. Cyto-ID Green/hoechst 33342 double staining and time-dependent experiment indicated that GMI and cisplatin-treated A549 cells simultaneously express autophagosomes and apoptotic nuclei. To elucidate the role of autophagy in inducing apoptosis by GMI and cisplatin, chemical inhibitors and LC3 shRNA were used to inhibit autophagy. The results showed that 3-methyladenine decreases, while chloroquine increases GMI and cisplatin cotreatment-induced cleavage of caspase-7 and PARP. LC3 silencing abolished activation of apoptosis in A549 cells. Caspase inhibitors and caspase-7 silencing mitigated GMI and cisplatin-elicited cell viability inhibition and apoptosis. This is the first study to reveal the novel function of GMI in potentiating cisplatin-mediated apoptosis. GMI and cisplatin induce apoptosis via autophagy/caspase-7-dependent and survivin- and ERCC1-independent pathway. GMI may be a potential cisplatin adjuvant against lung cancer.
DOI: 10.1021/mp500840z
PubMed: 25811903
Affiliations:
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Cells.</title><author><name sortKey="Hsin, I Lun" sort="Hsin, I Lun" uniqKey="Hsin I" first="I-Lun" last="Hsin">I-Lun Hsin</name><affiliation wicri:level="1"><nlm:affiliation>†Institute of Medicine, Chung Shan Medical University, Taichung 40203, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>†Institute of Medicine, Chung Shan Medical University, Taichung 40203</wicri:regionArea><wicri:noRegion>Taichung 40203</wicri:noRegion></affiliation></author><author><name sortKey="Ou, Chu Chyn" sort="Ou, Chu Chyn" uniqKey="Ou C" first="Chu-Chyn" last="Ou">Chu-Chyn Ou</name><affiliation wicri:level="1"><nlm:affiliation>‡School of Nutrition, Chung Shan Medical University, Taichung 40201, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>‡School of Nutrition, Chung Shan Medical University, Taichung 40201</wicri:regionArea><wicri:noRegion>Taichung 40201</wicri:noRegion></affiliation></author><author><name sortKey="Wu, Ming Fang" sort="Wu, Ming Fang" uniqKey="Wu M" first="Ming-Fang" last="Wu">Ming-Fang Wu</name><affiliation wicri:level="1"><nlm:affiliation>†Institute of Medicine, Chung Shan Medical University, Taichung 40203, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>†Institute of Medicine, Chung Shan Medical University, Taichung 40203</wicri:regionArea><wicri:noRegion>Taichung 40203</wicri:noRegion></affiliation></author><author><name sortKey="Jan, Ming Shiou" sort="Jan, Ming Shiou" uniqKey="Jan M" first="Ming-Shiou" last="Jan">Ming-Shiou Jan</name><affiliation wicri:level="1"><nlm:affiliation>¶Institute of Microbiology and Immunology, Chung Shan Medical University, Taichung 40201, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>¶Institute of Microbiology and Immunology, Chung Shan Medical University, Taichung 40201</wicri:regionArea><wicri:noRegion>Taichung 40201</wicri:noRegion></affiliation></author><author><name sortKey="Hsiao, Yi Min" sort="Hsiao, Yi Min" uniqKey="Hsiao Y" first="Yi-Min" last="Hsiao">Yi-Min Hsiao</name><affiliation wicri:level="1"><nlm:affiliation>∥Department of Medical Laboratory Science and Biotechnology, Central Taiwan University of Science and Technology, Taichung 40601, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>∥Department of Medical Laboratory Science and Biotechnology, Central Taiwan University of Science and Technology, Taichung 40601</wicri:regionArea><wicri:noRegion>Taichung 40601</wicri:noRegion></affiliation></author><author><name sortKey="Lin, Ching Hsiung" sort="Lin, Ching Hsiung" uniqKey="Lin C" first="Ching-Hsiung" last="Lin">Ching-Hsiung Lin</name><affiliation wicri:level="1"><nlm:affiliation>§School of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>§School of Medicine, Chung Shan Medical University, Taichung 40201</wicri:regionArea><wicri:noRegion>Taichung 40201</wicri:noRegion></affiliation></author><author><name sortKey="Ko, Jiunn Liang" sort="Ko, Jiunn Liang" uniqKey="Ko J" first="Jiunn-Liang" last="Ko">Jiunn-Liang Ko</name><affiliation wicri:level="1"><nlm:affiliation>†Institute of Medicine, Chung Shan Medical University, Taichung 40203, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>†Institute of Medicine, Chung Shan Medical University, Taichung 40203</wicri:regionArea><wicri:noRegion>Taichung 40203</wicri:noRegion></affiliation></author></analytic><series><title level="j">Molecular pharmaceutics</title><idno type="eISSN">1543-8392</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis (drug effects)</term><term>Autophagy (drug effects)</term><term>Caspase 3 (metabolism)</term><term>Caspase 7 (metabolism)</term><term>Cell Line</term><term>Cell Survival (drug effects)</term><term>Cisplatin (pharmacology)</term><term>Fungal Proteins (pharmacology)</term><term>Ganoderma (chemistry)</term><term>Humans</term><term>Lung Neoplasms (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Apoptose ()</term><term>Autophagie ()</term><term>Caspase-3 (métabolisme)</term><term>Caspase-7 (métabolisme)</term><term>Cisplatine (pharmacologie)</term><term>Ganoderma ()</term><term>Humains</term><term>Lignée cellulaire</term><term>Protéines fongiques (pharmacologie)</term><term>Survie cellulaire ()</term><term>Tumeurs du poumon (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Caspase 3</term><term>Caspase 7</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Ganoderma</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Autophagy</term><term>Cell Survival</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Caspase-3</term><term>Caspase-7</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Cisplatine</term><term>Protéines fongiques</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Cisplatin</term><term>Fungal Proteins</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Apoptose</term><term>Autophagie</term><term>Ganoderma</term><term>Humains</term><term>Lignée cellulaire</term><term>Survie cellulaire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Cisplatin-based therapy is common in the treatment of several types of cancers, including lung cancers. In our previous study, GMI, an immunomodulatory protein cloned from Ganoderma microsporum, induced a cytotoxic effect in lung cancer cells via autophagy. The aim of this study is to examine the role of GMI in enhancing cisplatin-mediated cell death. On the basis of MTT assay and Combination Index, GMI and cisplatin cotreatment induced a synergistic cytotoxic effect. GMI and cisplatin-induced apoptosis was determined by sub-G1, nuclear condensation, and annexin-V/propidium iodide analyses. On Western blot, expressions of γH2AX and cleaved forms of PARP, caspase-3, and caspase-7 were induced by combined treatment. Akt/mTOR pathway activity, LC3-II expression, and acidic vesicular organelle development demonstrated that cisplatin does not abolish GMI-mediated autophagy. Cyto-ID Green/hoechst 33342 double staining and time-dependent experiment indicated that GMI and cisplatin-treated A549 cells simultaneously express autophagosomes and apoptotic nuclei. To elucidate the role of autophagy in inducing apoptosis by GMI and cisplatin, chemical inhibitors and LC3 shRNA were used to inhibit autophagy. The results showed that 3-methyladenine decreases, while chloroquine increases GMI and cisplatin cotreatment-induced cleavage of caspase-7 and PARP. LC3 silencing abolished activation of apoptosis in A549 cells. Caspase inhibitors and caspase-7 silencing mitigated GMI and cisplatin-elicited cell viability inhibition and apoptosis. This is the first study to reveal the novel function of GMI in potentiating cisplatin-mediated apoptosis. GMI and cisplatin induce apoptosis via autophagy/caspase-7-dependent and survivin- and ERCC1-independent pathway. GMI may be a potential cisplatin adjuvant against lung cancer. </div></front></TEI><affiliations><list><country><li>Taïwan</li></country></list><tree><country name="Taïwan"><noRegion><name sortKey="Hsin, I Lun" sort="Hsin, I Lun" uniqKey="Hsin I" first="I-Lun" last="Hsin">I-Lun Hsin</name></noRegion><name sortKey="Hsiao, Yi Min" sort="Hsiao, Yi Min" uniqKey="Hsiao Y" first="Yi-Min" last="Hsiao">Yi-Min Hsiao</name><name sortKey="Jan, Ming Shiou" sort="Jan, Ming Shiou" uniqKey="Jan M" first="Ming-Shiou" last="Jan">Ming-Shiou Jan</name><name sortKey="Ko, Jiunn Liang" sort="Ko, Jiunn Liang" uniqKey="Ko J" first="Jiunn-Liang" last="Ko">Jiunn-Liang Ko</name><name sortKey="Lin, Ching Hsiung" sort="Lin, Ching Hsiung" uniqKey="Lin C" first="Ching-Hsiung" last="Lin">Ching-Hsiung Lin</name><name sortKey="Ou, Chu Chyn" sort="Ou, Chu Chyn" uniqKey="Ou C" first="Chu-Chyn" last="Ou">Chu-Chyn Ou</name><name sortKey="Wu, Ming Fang" sort="Wu, Ming Fang" uniqKey="Wu M" first="Ming-Fang" last="Wu">Ming-Fang Wu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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