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Anti-glioma action of aloe emodin: the role of ERK inhibition
The effect of aloe emodin (AE), a herbal anthraquinone derivative, on the rat C6 glioma cell line was investigated. In addition to cell cycle block and caspasedependent apoptosis, AE led to the formation of intracytoplasmic acidic vesicles indicative for autophagic cell death. Moreover, differentiat...
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| Published in: | Cellular and molecular life sciences : CMLS 2005-03, Vol.62 (5), p.589-598 |
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| container_title | Cellular and molecular life sciences : CMLS |
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| creator | Mijatovic, S Maksimovic-Ivanic, D Radovic, J Miljkovic, Dj Harhaji, Lj Vuckovic, O Stosic-Grujicic, S Mostarica Stojkovic, M Trajkovic, V |
| description | The effect of aloe emodin (AE), a herbal anthraquinone derivative, on the rat C6 glioma cell line was investigated. In addition to cell cycle block and caspasedependent apoptosis, AE led to the formation of intracytoplasmic acidic vesicles indicative for autophagic cell death. Moreover, differentiation of surviving cells toward the astrocytic lineage was confirmed by typical morphological changes and increased expression of glial fibrillary acidic protein (GFAP). AE did not affect the activation of mitogen-activated protein kinase p38, Jun-N-terminal kinase, or transcription factor NF-κB, but markedly inhibited the activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) in C6 cells. A selective inhibitor of ERK activation, PD98059, mimicked the effects of AE on glioma cell morphology and GFAP expression, but failed to induce either apoptosis or autophagy. Taken together, these results indicate that the anti-glioma action of AE involves ERK-independent induction of both apoptosis and autophagy, as well as ERK inhibition-mediated differentiation of glioma cells. |
| doi_str_mv | 10.1007/s00018-005-4425-8 |
| format | article |
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In addition to cell cycle block and caspasedependent apoptosis, AE led to the formation of intracytoplasmic acidic vesicles indicative for autophagic cell death. Moreover, differentiation of surviving cells toward the astrocytic lineage was confirmed by typical morphological changes and increased expression of glial fibrillary acidic protein (GFAP). AE did not affect the activation of mitogen-activated protein kinase p38, Jun-N-terminal kinase, or transcription factor NF-κB, but markedly inhibited the activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) in C6 cells. A selective inhibitor of ERK activation, PD98059, mimicked the effects of AE on glioma cell morphology and GFAP expression, but failed to induce either apoptosis or autophagy. Taken together, these results indicate that the anti-glioma action of AE involves ERK-independent induction of both apoptosis and autophagy, as well as ERK inhibition-mediated differentiation of glioma cells.</description><identifier>ISSN: 1420-682X</identifier><identifier>EISSN: 1420-9071</identifier><identifier>DOI: 10.1007/s00018-005-4425-8</identifier><identifier>PMID: 15747063</identifier><language>eng</language><publisher>Switzerland: Birkhäuser-Verlag</publisher><subject>Aloe ; Animals ; Anthraquinone ; Anthraquinones ; Antineoplastic Agents, Phytogenic - pharmacology ; Apoptosis ; Autolysis ; Autophagy ; Cell activation ; Cell cycle ; Cell death ; Cell differentiation ; Cell Differentiation - drug effects ; Cell Differentiation - physiology ; Cell Line, Tumor ; cell lines ; Cell morphology ; cell structures ; Cellular biology ; Differentiation ; Emodin ; Emodin - pharmacology ; Extracellular signal-regulated kinase ; Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors ; Extracellular Signal-Regulated MAP Kinases - physiology ; Glial fibrillary acidic protein ; glioma ; Glioma - enzymology ; Glioma cells ; Kinases ; MAP kinase ; mitogen-activated protein kinase ; Morphology ; NF-κB protein ; Proteins ; Rats ; Transcription activation ; transcription factor NF-kappa B ; transcription factors</subject><ispartof>Cellular and molecular life sciences : CMLS, 2005-03, Vol.62 (5), p.589-598</ispartof><rights>Birkhäuser Verlag, Basel 2005.</rights><rights>Birkhäuser Verlag, Basel 2005 2005</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-5ed74d010f868593605f57f8f144ef62ece30577899b6006f65d13a3e850eca03</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11365865/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11365865/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15747063$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mijatovic, S</creatorcontrib><creatorcontrib>Maksimovic-Ivanic, D</creatorcontrib><creatorcontrib>Radovic, J</creatorcontrib><creatorcontrib>Miljkovic, Dj</creatorcontrib><creatorcontrib>Harhaji, Lj</creatorcontrib><creatorcontrib>Vuckovic, O</creatorcontrib><creatorcontrib>Stosic-Grujicic, S</creatorcontrib><creatorcontrib>Mostarica Stojkovic, M</creatorcontrib><creatorcontrib>Trajkovic, V</creatorcontrib><title>Anti-glioma action of aloe emodin: the role of ERK inhibition</title><title>Cellular and molecular life sciences : CMLS</title><addtitle>Cell Mol Life Sci</addtitle><description>The effect of aloe emodin (AE), a herbal anthraquinone derivative, on the rat C6 glioma cell line was investigated. In addition to cell cycle block and caspasedependent apoptosis, AE led to the formation of intracytoplasmic acidic vesicles indicative for autophagic cell death. Moreover, differentiation of surviving cells toward the astrocytic lineage was confirmed by typical morphological changes and increased expression of glial fibrillary acidic protein (GFAP). AE did not affect the activation of mitogen-activated protein kinase p38, Jun-N-terminal kinase, or transcription factor NF-κB, but markedly inhibited the activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) in C6 cells. A selective inhibitor of ERK activation, PD98059, mimicked the effects of AE on glioma cell morphology and GFAP expression, but failed to induce either apoptosis or autophagy. Taken together, these results indicate that the anti-glioma action of AE involves ERK-independent induction of both apoptosis and autophagy, as well as ERK inhibition-mediated differentiation of glioma cells.</description><subject>Aloe</subject><subject>Animals</subject><subject>Anthraquinone</subject><subject>Anthraquinones</subject><subject>Antineoplastic Agents, Phytogenic - pharmacology</subject><subject>Apoptosis</subject><subject>Autolysis</subject><subject>Autophagy</subject><subject>Cell activation</subject><subject>Cell cycle</subject><subject>Cell death</subject><subject>Cell differentiation</subject><subject>Cell Differentiation - drug effects</subject><subject>Cell Differentiation - physiology</subject><subject>Cell Line, Tumor</subject><subject>cell lines</subject><subject>Cell morphology</subject><subject>cell structures</subject><subject>Cellular biology</subject><subject>Differentiation</subject><subject>Emodin</subject><subject>Emodin - pharmacology</subject><subject>Extracellular signal-regulated kinase</subject><subject>Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors</subject><subject>Extracellular Signal-Regulated MAP Kinases - physiology</subject><subject>Glial fibrillary acidic protein</subject><subject>glioma</subject><subject>Glioma - enzymology</subject><subject>Glioma cells</subject><subject>Kinases</subject><subject>MAP kinase</subject><subject>mitogen-activated protein kinase</subject><subject>Morphology</subject><subject>NF-κB protein</subject><subject>Proteins</subject><subject>Rats</subject><subject>Transcription activation</subject><subject>transcription factor NF-kappa B</subject><subject>transcription 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action of aloe emodin: the role of ERK inhibition</title><author>Mijatovic, S ; Maksimovic-Ivanic, D ; Radovic, J ; Miljkovic, Dj ; Harhaji, Lj ; Vuckovic, O ; Stosic-Grujicic, S ; Mostarica Stojkovic, M ; Trajkovic, V</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-5ed74d010f868593605f57f8f144ef62ece30577899b6006f65d13a3e850eca03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Aloe</topic><topic>Animals</topic><topic>Anthraquinone</topic><topic>Anthraquinones</topic><topic>Antineoplastic Agents, Phytogenic - pharmacology</topic><topic>Apoptosis</topic><topic>Autolysis</topic><topic>Autophagy</topic><topic>Cell activation</topic><topic>Cell cycle</topic><topic>Cell death</topic><topic>Cell differentiation</topic><topic>Cell Differentiation - drug effects</topic><topic>Cell Differentiation - physiology</topic><topic>Cell Line, Tumor</topic><topic>cell 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In addition to cell cycle block and caspasedependent apoptosis, AE led to the formation of intracytoplasmic acidic vesicles indicative for autophagic cell death. Moreover, differentiation of surviving cells toward the astrocytic lineage was confirmed by typical morphological changes and increased expression of glial fibrillary acidic protein (GFAP). AE did not affect the activation of mitogen-activated protein kinase p38, Jun-N-terminal kinase, or transcription factor NF-κB, but markedly inhibited the activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) in C6 cells. A selective inhibitor of ERK activation, PD98059, mimicked the effects of AE on glioma cell morphology and GFAP expression, but failed to induce either apoptosis or autophagy. Taken together, these results indicate that the anti-glioma action of AE involves ERK-independent induction of both apoptosis and autophagy, as well as ERK inhibition-mediated differentiation of glioma cells.</abstract><cop>Switzerland</cop><pub>Birkhäuser-Verlag</pub><pmid>15747063</pmid><doi>10.1007/s00018-005-4425-8</doi><tpages>10</tpages></addata></record> |
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| subjects | Aloe Animals Anthraquinone Anthraquinones Antineoplastic Agents, Phytogenic - pharmacology Apoptosis Autolysis Autophagy Cell activation Cell cycle Cell death Cell differentiation Cell Differentiation - drug effects Cell Differentiation - physiology Cell Line, Tumor cell lines Cell morphology cell structures Cellular biology Differentiation Emodin Emodin - pharmacology Extracellular signal-regulated kinase Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors Extracellular Signal-Regulated MAP Kinases - physiology Glial fibrillary acidic protein glioma Glioma - enzymology Glioma cells Kinases MAP kinase mitogen-activated protein kinase Morphology NF-κB protein Proteins Rats Transcription activation transcription factor NF-kappa B transcription factors |
| title | Anti-glioma action of aloe emodin: the role of ERK inhibition |
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