Bruceine D induces lung cancer cell apoptosis and autophagy via the ROS/MAPK signaling pathway in vitro and in vivo
Worldwide, lung cancer remains a leading cause of cancer mortality. Bruceine D (BD) has been shown to induce pancreatic cancer cell death via several different mechanisms. In this study, we demonstrated that BD inhibited lung cancer cell proliferation. Apoptosis and autophagy were the most important...
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| Veröffentlicht in: | Cell death & disease 2020-02, Vol.11 (2), p.126-126, Article 126 |
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| creator | Fan, Jiangjiang Ren, Dongmei Wang, Jinxia Liu, Xiaoqing Zhang, Huaran Wu, Mingsheng Yang, Guotao |
| description | Worldwide, lung cancer remains a leading cause of cancer mortality. Bruceine D (BD) has been shown to induce pancreatic cancer cell death via several different mechanisms. In this study, we demonstrated that BD inhibited lung cancer cell proliferation. Apoptosis and autophagy were the most important mechanisms involved in BD-induced lung cancer cell death, and complete autophagic flux was observed in A549 and NCI-H292 cells. In addition, BD significantly improved intracellular reactive oxygen species (ROS) levels. BD-mediated cell apoptosis and autophagy were almost inhibited in cells pretreated with N-acetylcysteine (NAC), an ROS scavenger. Furthermore, MAPK signaling pathway activation contributed to BD-induced cell proliferation inhibition and NAC could eliminate p-ERK and p-JNK upregulation. Finally, an in vivo study indicated that BD inhibited the growth of lung cancer xenografts. Overall, BD is a promising candidate for the treatment of lung cancer owing to its multiple mechanisms and low toxicity. |
| doi_str_mv | 10.1038/s41419-020-2317-3 |
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Bruceine D (BD) has been shown to induce pancreatic cancer cell death via several different mechanisms. In this study, we demonstrated that BD inhibited lung cancer cell proliferation. Apoptosis and autophagy were the most important mechanisms involved in BD-induced lung cancer cell death, and complete autophagic flux was observed in A549 and NCI-H292 cells. In addition, BD significantly improved intracellular reactive oxygen species (ROS) levels. BD-mediated cell apoptosis and autophagy were almost inhibited in cells pretreated with N-acetylcysteine (NAC), an ROS scavenger. Furthermore, MAPK signaling pathway activation contributed to BD-induced cell proliferation inhibition and NAC could eliminate p-ERK and p-JNK upregulation. Finally, an in vivo study indicated that BD inhibited the growth of lung cancer xenografts. Overall, BD is a promising candidate for the treatment of lung cancer owing to its multiple mechanisms and low toxicity.</description><identifier>ISSN: 2041-4889</identifier><identifier>EISSN: 2041-4889</identifier><identifier>DOI: 10.1038/s41419-020-2317-3</identifier><identifier>PMID: 32071301</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/109 ; 13/2 ; 13/31 ; 14/19 ; 14/28 ; 14/34 ; 14/35 ; 14/63 ; 631/154/570 ; 631/67/1612/1350 ; 631/80/39 ; 64/60 ; 82/80 ; A549 Cells ; Acetylcysteine ; Animals ; Antibodies ; Antineoplastic Agents, Phytogenic - pharmacology ; Apoptosis ; Apoptosis - drug effects ; Autophagy ; Autophagy - drug effects ; Biochemistry ; Biomedical and Life Sciences ; Cell activation ; Cell Biology ; Cell Culture ; Cell death ; Cell growth ; Cell proliferation ; Cell Proliferation - drug effects ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Female ; Humans ; Immunology ; JNK Mitogen-Activated Protein Kinases - metabolism ; Life Sciences ; Lung cancer ; Lung Neoplasms - drug therapy ; Lung Neoplasms - enzymology ; Lung Neoplasms - pathology ; MAP kinase ; MAP Kinase Signaling System - drug effects ; Mice, Inbred BALB C ; Mice, Nude ; Pancreatic cancer ; Phagocytosis ; Phosphorylation ; Quassins - pharmacology ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Signal transduction ; Toxicity ; Tumor Burden - drug effects ; Xenograft Model Antitumor Assays ; Xenografts</subject><ispartof>Cell death & disease, 2020-02, Vol.11 (2), p.126-126, Article 126</ispartof><rights>The Author(s) 2020</rights><rights>This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c536t-97abb1cd6c50ff637c8ce97e69677294bd8f28726ae6028eda7500658f3c19ca3</citedby><cites>FETCH-LOGICAL-c536t-97abb1cd6c50ff637c8ce97e69677294bd8f28726ae6028eda7500658f3c19ca3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7028916/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7028916/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32071301$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fan, Jiangjiang</creatorcontrib><creatorcontrib>Ren, Dongmei</creatorcontrib><creatorcontrib>Wang, Jinxia</creatorcontrib><creatorcontrib>Liu, Xiaoqing</creatorcontrib><creatorcontrib>Zhang, Huaran</creatorcontrib><creatorcontrib>Wu, Mingsheng</creatorcontrib><creatorcontrib>Yang, Guotao</creatorcontrib><title>Bruceine D induces lung cancer cell apoptosis and autophagy via the ROS/MAPK signaling pathway in vitro and in vivo</title><title>Cell death & disease</title><addtitle>Cell Death Dis</addtitle><addtitle>Cell Death Dis</addtitle><description>Worldwide, lung cancer remains a leading cause of cancer mortality. Bruceine D (BD) has been shown to induce pancreatic cancer cell death via several different mechanisms. In this study, we demonstrated that BD inhibited lung cancer cell proliferation. Apoptosis and autophagy were the most important mechanisms involved in BD-induced lung cancer cell death, and complete autophagic flux was observed in A549 and NCI-H292 cells. In addition, BD significantly improved intracellular reactive oxygen species (ROS) levels. BD-mediated cell apoptosis and autophagy were almost inhibited in cells pretreated with N-acetylcysteine (NAC), an ROS scavenger. Furthermore, MAPK signaling pathway activation contributed to BD-induced cell proliferation inhibition and NAC could eliminate p-ERK and p-JNK upregulation. Finally, an in vivo study indicated that BD inhibited the growth of lung cancer xenografts. Overall, BD is a promising candidate for the treatment of lung cancer owing to its multiple mechanisms and low toxicity.</description><subject>13/109</subject><subject>13/2</subject><subject>13/31</subject><subject>14/19</subject><subject>14/28</subject><subject>14/34</subject><subject>14/35</subject><subject>14/63</subject><subject>631/154/570</subject><subject>631/67/1612/1350</subject><subject>631/80/39</subject><subject>64/60</subject><subject>82/80</subject><subject>A549 Cells</subject><subject>Acetylcysteine</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Antineoplastic Agents, Phytogenic - pharmacology</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Autophagy</subject><subject>Autophagy - drug effects</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cell activation</subject><subject>Cell Biology</subject><subject>Cell Culture</subject><subject>Cell death</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell death & disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fan, Jiangjiang</au><au>Ren, Dongmei</au><au>Wang, Jinxia</au><au>Liu, Xiaoqing</au><au>Zhang, Huaran</au><au>Wu, Mingsheng</au><au>Yang, Guotao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bruceine D induces lung cancer cell apoptosis and autophagy via the ROS/MAPK signaling pathway in vitro and in vivo</atitle><jtitle>Cell death & disease</jtitle><stitle>Cell Death Dis</stitle><addtitle>Cell Death Dis</addtitle><date>2020-02-18</date><risdate>2020</risdate><volume>11</volume><issue>2</issue><spage>126</spage><epage>126</epage><pages>126-126</pages><artnum>126</artnum><issn>2041-4889</issn><eissn>2041-4889</eissn><abstract>Worldwide, lung cancer remains a leading cause of cancer mortality. Bruceine D (BD) has been shown to induce pancreatic cancer cell death via several different mechanisms. In this study, we demonstrated that BD inhibited lung cancer cell proliferation. Apoptosis and autophagy were the most important mechanisms involved in BD-induced lung cancer cell death, and complete autophagic flux was observed in A549 and NCI-H292 cells. In addition, BD significantly improved intracellular reactive oxygen species (ROS) levels. BD-mediated cell apoptosis and autophagy were almost inhibited in cells pretreated with N-acetylcysteine (NAC), an ROS scavenger. Furthermore, MAPK signaling pathway activation contributed to BD-induced cell proliferation inhibition and NAC could eliminate p-ERK and p-JNK upregulation. Finally, an in vivo study indicated that BD inhibited the growth of lung cancer xenografts. Overall, BD is a promising candidate for the treatment of lung cancer owing to its multiple mechanisms and low toxicity.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>32071301</pmid><doi>10.1038/s41419-020-2317-3</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13/109 13/2 13/31 14/19 14/28 14/34 14/35 14/63 631/154/570 631/67/1612/1350 631/80/39 64/60 82/80 A549 Cells Acetylcysteine Animals Antibodies Antineoplastic Agents, Phytogenic - pharmacology Apoptosis Apoptosis - drug effects Autophagy Autophagy - drug effects Biochemistry Biomedical and Life Sciences Cell activation Cell Biology Cell Culture Cell death Cell growth Cell proliferation Cell Proliferation - drug effects Extracellular Signal-Regulated MAP Kinases - metabolism Female Humans Immunology JNK Mitogen-Activated Protein Kinases - metabolism Life Sciences Lung cancer Lung Neoplasms - drug therapy Lung Neoplasms - enzymology Lung Neoplasms - pathology MAP kinase MAP Kinase Signaling System - drug effects Mice, Inbred BALB C Mice, Nude Pancreatic cancer Phagocytosis Phosphorylation Quassins - pharmacology Reactive oxygen species Reactive Oxygen Species - metabolism Signal transduction Toxicity Tumor Burden - drug effects Xenograft Model Antitumor Assays Xenografts |
| title | Bruceine D induces lung cancer cell apoptosis and autophagy via the ROS/MAPK signaling pathway in vitro and in vivo |
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