Apoptosis induced by bruceine D in human non‑small‑cell lung cancer cells involves mitochondrial ROS‑mediated death signaling
Bruceine D is one of the active components of Brucea javanica (L.) Merr., which is widely used to treat cancer in China. The aim of the present study was to evaluate the potential effect of bruceine D against non‑small‑cell lung cancer (NSCLC) cells and delineate its underlying mechanisms. The resul...
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| Veröffentlicht in: | International journal of molecular medicine 2019-12, Vol.44 (6), p.2015-2026 |
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| creator | Xie, Jian-Hui Lai, Zheng-Quan Zheng, Xing-Han Xian, Yan-Fang Li, Qian Ip, Siu-Po Xie, You-Liang Chen, Jian-Nan Su, Zi-Ren Lin, Zhi-Xiu Yang, Xiao-Bo |
| description | Bruceine D is one of the active components of Brucea javanica (L.) Merr., which is widely used to treat cancer in China. The aim of the present study was to evaluate the potential effect of bruceine D against non‑small‑cell lung cancer (NSCLC) cells and delineate its underlying mechanisms. The results indicated that treatment with bruceine D markedly inhibited the proliferation of wild‑type NSCLC cells and epidermal growth factor receptor‑mutant cells in a dose‑ and time‑dependent manner, and significantly decreased the colony‑forming ability and migration of A549 cells. Hoechst 33342 staining and flow cytometric analysis demonstrated that treatment with bruceine D effectively induced apoptosis of A549 cells. In addition, the proapoptotic effect of bruceine D was found to be associated with G0‑G1 cell cycle arrest, accumulation of intracellular reactive oxygen species (ROS) and malondialdehyde, depletion of glutathione levels and disruption of mitochondrial membrane potential. Additionally, pretreatment with N‑acetylcysteine, a ROS scavenger, significantly attenuated the bruceine D‑induced inhibition in A549 cells. Western blotting demonstrated that treatment with bruceine D significantly suppressed the expression of the anti‑apoptotic proteins Bcl‑2, Bcl‑xL and X‑linked inhibitor of apoptosis, enhanced the expression levels of apoptotic proteins Bax and Bak, and inhibited the expression of pro‑caspase‑3 and pro‑caspase‑8. Based on these results, it may be suggested that inhibition of A549 NSCLC cell proliferation by bruceine D is associated with the modulation of ROS‑mitochondrial‑mediated death signaling. This novel insight may provide further evidence to verify the anticancer efficacy of B. javanica, and support a role for bruceine D in the anti‑NSCLC treatment. |
| doi_str_mv | 10.3892/ijmm.2019.4363 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6844635</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A606944555</galeid><sourcerecordid>A606944555</sourcerecordid><originalsourceid>FETCH-LOGICAL-c485t-67922869f70e01ad7e1676be7851612a3102451bb5cd72dafaeb75cca71370df3</originalsourceid><addsrcrecordid>eNptUsuKFDEULURxxtGtSwm4rjbvpDZCMz5hYMAHuAupJFWdJpW0SVXD7Fz4A_6B3-Kn-CWmcBwVhizu5eSck3vJaZrHCG6I7PAzv5-mDYao21DCyZ3mFIkOtZjST3drj6BoiWD8pHlQyh5CzGgn7zcnBHEikUSnzdftIR3mVHwBPtrFOAv6K9Dn2vnofnx_UWGwWyYdQUzx55dvZdIh1GpcCCAscQRGR-MyWIHV5JjC0RUw-TmZXYo2ex3Au8v3VTM56_Vcn7BOzztQ_Bh18HF82NwbdCju0XU9az6-evnh_E17cfn67fn2ojVUsrnlosNY8m4Q0EGkrXCIC947IRniCGuCIKYM9T0zVmCrB-16wYzRAhEB7UDOmue_fQ9LX2cxLs5ZB3XIftL5SiXt1f830e_UmI6KS0o5YdXg6bVBTp8XV2a1T0uuSxSFCSId7jCRf1mjDk75OKRqZiZfjNpyyDtKGVu9Nrew6rFu8iZFN_iK3yYwOZWS3XAzOIJqDYNaw6DWMKg1DFXw5N91b-h_fp_8Ao5wte4</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2313929238</pqid></control><display><type>article</type><title>Apoptosis induced by bruceine D in human non‑small‑cell lung cancer cells involves mitochondrial ROS‑mediated death signaling</title><source>Spandidos Publications Journals</source><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Xie, Jian-Hui ; Lai, Zheng-Quan ; Zheng, Xing-Han ; Xian, Yan-Fang ; Li, Qian ; Ip, Siu-Po ; Xie, You-Liang ; Chen, Jian-Nan ; Su, Zi-Ren ; Lin, Zhi-Xiu ; Yang, Xiao-Bo</creator><creatorcontrib>Xie, Jian-Hui ; Lai, Zheng-Quan ; Zheng, Xing-Han ; Xian, Yan-Fang ; Li, Qian ; Ip, Siu-Po ; Xie, You-Liang ; Chen, Jian-Nan ; Su, Zi-Ren ; Lin, Zhi-Xiu ; Yang, Xiao-Bo</creatorcontrib><description>Bruceine D is one of the active components of Brucea javanica (L.) Merr., which is widely used to treat cancer in China. The aim of the present study was to evaluate the potential effect of bruceine D against non‑small‑cell lung cancer (NSCLC) cells and delineate its underlying mechanisms. The results indicated that treatment with bruceine D markedly inhibited the proliferation of wild‑type NSCLC cells and epidermal growth factor receptor‑mutant cells in a dose‑ and time‑dependent manner, and significantly decreased the colony‑forming ability and migration of A549 cells. Hoechst 33342 staining and flow cytometric analysis demonstrated that treatment with bruceine D effectively induced apoptosis of A549 cells. In addition, the proapoptotic effect of bruceine D was found to be associated with G0‑G1 cell cycle arrest, accumulation of intracellular reactive oxygen species (ROS) and malondialdehyde, depletion of glutathione levels and disruption of mitochondrial membrane potential. Additionally, pretreatment with N‑acetylcysteine, a ROS scavenger, significantly attenuated the bruceine D‑induced inhibition in A549 cells. Western blotting demonstrated that treatment with bruceine D significantly suppressed the expression of the anti‑apoptotic proteins Bcl‑2, Bcl‑xL and X‑linked inhibitor of apoptosis, enhanced the expression levels of apoptotic proteins Bax and Bak, and inhibited the expression of pro‑caspase‑3 and pro‑caspase‑8. Based on these results, it may be suggested that inhibition of A549 NSCLC cell proliferation by bruceine D is associated with the modulation of ROS‑mitochondrial‑mediated death signaling. This novel insight may provide further evidence to verify the anticancer efficacy of B. javanica, and support a role for bruceine D in the anti‑NSCLC treatment.</description><identifier>ISSN: 1107-3756</identifier><identifier>EISSN: 1791-244X</identifier><identifier>DOI: 10.3892/ijmm.2019.4363</identifier><identifier>PMID: 31638181</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>A549 Cells ; Acetylcysteine ; Apoptosis ; Apoptosis - drug effects ; Cancer cells ; Cancer therapies ; Carcinoma, Non-Small-Cell Lung - drug therapy ; Carcinoma, Non-Small-Cell Lung - genetics ; Carcinoma, Non-Small-Cell Lung - pathology ; Cell cycle ; Cell Cycle Checkpoints - drug effects ; Cell Movement - drug effects ; Cell Proliferation - drug effects ; Cytotoxicity ; Epidermal growth factors ; Gene Expression Regulation, Neoplastic - drug effects ; Humans ; Instrument industry (Equipment) ; Laboratories ; Lung cancer ; Medicine ; Membrane Potential, Mitochondrial - drug effects ; Mitochondria ; Mitochondria - drug effects ; NMR ; Non-small cell lung cancer ; Novels ; Nuclear magnetic resonance ; Protein expression ; Proteins ; Proto-Oncogene Proteins c-bcl-2 - genetics ; Quassins - pharmacology ; Reactive Oxygen Species - metabolism ; Scientific equipment industry ; Signal Transduction - drug effects ; Studies</subject><ispartof>International journal of molecular medicine, 2019-12, Vol.44 (6), p.2015-2026</ispartof><rights>COPYRIGHT 2019 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2019</rights><rights>Copyright: © Xie et al. 2019</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c485t-67922869f70e01ad7e1676be7851612a3102451bb5cd72dafaeb75cca71370df3</citedby><cites>FETCH-LOGICAL-c485t-67922869f70e01ad7e1676be7851612a3102451bb5cd72dafaeb75cca71370df3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,781,785,886,27929,27930</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31638181$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xie, Jian-Hui</creatorcontrib><creatorcontrib>Lai, Zheng-Quan</creatorcontrib><creatorcontrib>Zheng, Xing-Han</creatorcontrib><creatorcontrib>Xian, Yan-Fang</creatorcontrib><creatorcontrib>Li, Qian</creatorcontrib><creatorcontrib>Ip, Siu-Po</creatorcontrib><creatorcontrib>Xie, You-Liang</creatorcontrib><creatorcontrib>Chen, Jian-Nan</creatorcontrib><creatorcontrib>Su, Zi-Ren</creatorcontrib><creatorcontrib>Lin, Zhi-Xiu</creatorcontrib><creatorcontrib>Yang, Xiao-Bo</creatorcontrib><title>Apoptosis induced by bruceine D in human non‑small‑cell lung cancer cells involves mitochondrial ROS‑mediated death signaling</title><title>International journal of molecular medicine</title><addtitle>Int J Mol Med</addtitle><description>Bruceine D is one of the active components of Brucea javanica (L.) Merr., which is widely used to treat cancer in China. The aim of the present study was to evaluate the potential effect of bruceine D against non‑small‑cell lung cancer (NSCLC) cells and delineate its underlying mechanisms. The results indicated that treatment with bruceine D markedly inhibited the proliferation of wild‑type NSCLC cells and epidermal growth factor receptor‑mutant cells in a dose‑ and time‑dependent manner, and significantly decreased the colony‑forming ability and migration of A549 cells. Hoechst 33342 staining and flow cytometric analysis demonstrated that treatment with bruceine D effectively induced apoptosis of A549 cells. In addition, the proapoptotic effect of bruceine D was found to be associated with G0‑G1 cell cycle arrest, accumulation of intracellular reactive oxygen species (ROS) and malondialdehyde, depletion of glutathione levels and disruption of mitochondrial membrane potential. Additionally, pretreatment with N‑acetylcysteine, a ROS scavenger, significantly attenuated the bruceine D‑induced inhibition in A549 cells. Western blotting demonstrated that treatment with bruceine D significantly suppressed the expression of the anti‑apoptotic proteins Bcl‑2, Bcl‑xL and X‑linked inhibitor of apoptosis, enhanced the expression levels of apoptotic proteins Bax and Bak, and inhibited the expression of pro‑caspase‑3 and pro‑caspase‑8. Based on these results, it may be suggested that inhibition of A549 NSCLC cell proliferation by bruceine D is associated with the modulation of ROS‑mitochondrial‑mediated death signaling. This novel insight may provide further evidence to verify the anticancer efficacy of B. javanica, and support a role for bruceine D in the anti‑NSCLC treatment.</description><subject>A549 Cells</subject><subject>Acetylcysteine</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Cancer cells</subject><subject>Cancer therapies</subject><subject>Carcinoma, Non-Small-Cell Lung - drug therapy</subject><subject>Carcinoma, Non-Small-Cell Lung - genetics</subject><subject>Carcinoma, Non-Small-Cell Lung - pathology</subject><subject>Cell cycle</subject><subject>Cell Cycle Checkpoints - drug effects</subject><subject>Cell Movement - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Cytotoxicity</subject><subject>Epidermal growth factors</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Humans</subject><subject>Instrument industry (Equipment)</subject><subject>Laboratories</subject><subject>Lung cancer</subject><subject>Medicine</subject><subject>Membrane Potential, Mitochondrial - drug effects</subject><subject>Mitochondria</subject><subject>Mitochondria - drug effects</subject><subject>NMR</subject><subject>Non-small cell lung cancer</subject><subject>Novels</subject><subject>Nuclear magnetic resonance</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-bcl-2 - genetics</subject><subject>Quassins - pharmacology</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Scientific equipment industry</subject><subject>Signal Transduction - drug effects</subject><subject>Studies</subject><issn>1107-3756</issn><issn>1791-244X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptUsuKFDEULURxxtGtSwm4rjbvpDZCMz5hYMAHuAupJFWdJpW0SVXD7Fz4A_6B3-Kn-CWmcBwVhizu5eSck3vJaZrHCG6I7PAzv5-mDYao21DCyZ3mFIkOtZjST3drj6BoiWD8pHlQyh5CzGgn7zcnBHEikUSnzdftIR3mVHwBPtrFOAv6K9Dn2vnofnx_UWGwWyYdQUzx55dvZdIh1GpcCCAscQRGR-MyWIHV5JjC0RUw-TmZXYo2ex3Au8v3VTM56_Vcn7BOzztQ_Bh18HF82NwbdCju0XU9az6-evnh_E17cfn67fn2ojVUsrnlosNY8m4Q0EGkrXCIC947IRniCGuCIKYM9T0zVmCrB-16wYzRAhEB7UDOmue_fQ9LX2cxLs5ZB3XIftL5SiXt1f830e_UmI6KS0o5YdXg6bVBTp8XV2a1T0uuSxSFCSId7jCRf1mjDk75OKRqZiZfjNpyyDtKGVu9Nrew6rFu8iZFN_iK3yYwOZWS3XAzOIJqDYNaw6DWMKg1DFXw5N91b-h_fp_8Ao5wte4</recordid><startdate>20191201</startdate><enddate>20191201</enddate><creator>Xie, Jian-Hui</creator><creator>Lai, Zheng-Quan</creator><creator>Zheng, Xing-Han</creator><creator>Xian, Yan-Fang</creator><creator>Li, Qian</creator><creator>Ip, Siu-Po</creator><creator>Xie, You-Liang</creator><creator>Chen, Jian-Nan</creator><creator>Su, Zi-Ren</creator><creator>Lin, Zhi-Xiu</creator><creator>Yang, Xiao-Bo</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. 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drug effects</topic><topic>Cancer cells</topic><topic>Cancer therapies</topic><topic>Carcinoma, Non-Small-Cell Lung - drug therapy</topic><topic>Carcinoma, Non-Small-Cell Lung - genetics</topic><topic>Carcinoma, Non-Small-Cell Lung - pathology</topic><topic>Cell cycle</topic><topic>Cell Cycle Checkpoints - drug effects</topic><topic>Cell Movement - drug effects</topic><topic>Cell Proliferation - drug effects</topic><topic>Cytotoxicity</topic><topic>Epidermal growth factors</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Humans</topic><topic>Instrument industry (Equipment)</topic><topic>Laboratories</topic><topic>Lung cancer</topic><topic>Medicine</topic><topic>Membrane Potential, Mitochondrial - drug effects</topic><topic>Mitochondria</topic><topic>Mitochondria - drug effects</topic><topic>NMR</topic><topic>Non-small cell lung cancer</topic><topic>Novels</topic><topic>Nuclear magnetic resonance</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-bcl-2 - 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Merr., which is widely used to treat cancer in China. The aim of the present study was to evaluate the potential effect of bruceine D against non‑small‑cell lung cancer (NSCLC) cells and delineate its underlying mechanisms. The results indicated that treatment with bruceine D markedly inhibited the proliferation of wild‑type NSCLC cells and epidermal growth factor receptor‑mutant cells in a dose‑ and time‑dependent manner, and significantly decreased the colony‑forming ability and migration of A549 cells. Hoechst 33342 staining and flow cytometric analysis demonstrated that treatment with bruceine D effectively induced apoptosis of A549 cells. In addition, the proapoptotic effect of bruceine D was found to be associated with G0‑G1 cell cycle arrest, accumulation of intracellular reactive oxygen species (ROS) and malondialdehyde, depletion of glutathione levels and disruption of mitochondrial membrane potential. Additionally, pretreatment with N‑acetylcysteine, a ROS scavenger, significantly attenuated the bruceine D‑induced inhibition in A549 cells. Western blotting demonstrated that treatment with bruceine D significantly suppressed the expression of the anti‑apoptotic proteins Bcl‑2, Bcl‑xL and X‑linked inhibitor of apoptosis, enhanced the expression levels of apoptotic proteins Bax and Bak, and inhibited the expression of pro‑caspase‑3 and pro‑caspase‑8. Based on these results, it may be suggested that inhibition of A549 NSCLC cell proliferation by bruceine D is associated with the modulation of ROS‑mitochondrial‑mediated death signaling. This novel insight may provide further evidence to verify the anticancer efficacy of B. javanica, and support a role for bruceine D in the anti‑NSCLC treatment.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>31638181</pmid><doi>10.3892/ijmm.2019.4363</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | A549 Cells Acetylcysteine Apoptosis Apoptosis - drug effects Cancer cells Cancer therapies Carcinoma, Non-Small-Cell Lung - drug therapy Carcinoma, Non-Small-Cell Lung - genetics Carcinoma, Non-Small-Cell Lung - pathology Cell cycle Cell Cycle Checkpoints - drug effects Cell Movement - drug effects Cell Proliferation - drug effects Cytotoxicity Epidermal growth factors Gene Expression Regulation, Neoplastic - drug effects Humans Instrument industry (Equipment) Laboratories Lung cancer Medicine Membrane Potential, Mitochondrial - drug effects Mitochondria Mitochondria - drug effects NMR Non-small cell lung cancer Novels Nuclear magnetic resonance Protein expression Proteins Proto-Oncogene Proteins c-bcl-2 - genetics Quassins - pharmacology Reactive Oxygen Species - metabolism Scientific equipment industry Signal Transduction - drug effects Studies |
| title | Apoptosis induced by bruceine D in human non‑small‑cell lung cancer cells involves mitochondrial ROS‑mediated death signaling |
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