Icariin inhibits proliferation, migration, and invasion of medulloblastoma DAOY cells by regulation of SPARC.
Identifieur interne : 000080 ( Main/Exploration ); précédent : 000079; suivant : 000081Icariin inhibits proliferation, migration, and invasion of medulloblastoma DAOY cells by regulation of SPARC.
Auteurs : Yan Yang [République populaire de Chine] ; Guifang Li [République populaire de Chine]Source :
- Phytotherapy research : PTR [ 1099-1573 ] ; 2020.
Descripteurs français
- KwdFr :
- Antinéoplasiques d'origine végétale (pharmacologie), Apoptose (effets des médicaments et des substances chimiques), Facteur de transcription STAT-3 (génétique), Facteur de transcription STAT-3 (métabolisme), Flavonoïdes (pharmacologie), Humains (MeSH), Invasion tumorale (prévention et contrôle), Janus kinase 1 (génétique), Janus kinase 1 (métabolisme), Lignée cellulaire tumorale (MeSH), Mouvement cellulaire (effets des médicaments et des substances chimiques), Médulloblastome (traitement médicamenteux), Ostéonectine (génétique), Ostéonectine (métabolisme), Phosphatidylinositol 3-kinases (génétique), Phosphatidylinositol 3-kinases (métabolisme), Prolifération cellulaire (effets des médicaments et des substances chimiques), Protéine oncogène v-akt (génétique), Protéine oncogène v-akt (métabolisme), Régulation de l'expression des gènes tumoraux (effets des médicaments et des substances chimiques), Survie cellulaire (effets des médicaments et des substances chimiques), Tumeurs du cervelet (traitement médicamenteux).
- MESH :
- effets des médicaments et des substances chimiques : Apoptose, Mouvement cellulaire, Prolifération cellulaire, Régulation de l'expression des gènes tumoraux, Survie cellulaire.
- génétique : Facteur de transcription STAT-3, Janus kinase 1, Ostéonectine, Phosphatidylinositol 3-kinases, Protéine oncogène v-akt.
- métabolisme : Facteur de transcription STAT-3, Janus kinase 1, Ostéonectine, Phosphatidylinositol 3-kinases, Protéine oncogène v-akt.
- pharmacologie : Antinéoplasiques d'origine végétale, Flavonoïdes.
- prévention et contrôle : Invasion tumorale.
- traitement médicamenteux : Médulloblastome, Tumeurs du cervelet.
- Humains, Lignée cellulaire tumorale.
English descriptors
- KwdEn :
- Antineoplastic Agents, Phytogenic (pharmacology), Apoptosis (drug effects), Cell Line, Tumor (MeSH), Cell Movement (drug effects), Cell Proliferation (drug effects), Cell Survival (drug effects), Cerebellar Neoplasms (drug therapy), Flavonoids (pharmacology), Gene Expression Regulation, Neoplastic (drug effects), Humans (MeSH), Janus Kinase 1 (genetics), Janus Kinase 1 (metabolism), Medulloblastoma (drug therapy), Neoplasm Invasiveness (prevention & control), Oncogene Protein v-akt (genetics), Oncogene Protein v-akt (metabolism), Osteonectin (genetics), Osteonectin (metabolism), Phosphatidylinositol 3-Kinases (genetics), Phosphatidylinositol 3-Kinases (metabolism), STAT3 Transcription Factor (genetics), STAT3 Transcription Factor (metabolism).
- MESH :
- chemical , genetics : Janus Kinase 1, Oncogene Protein v-akt, Osteonectin, STAT3 Transcription Factor.
- chemical , metabolism : Janus Kinase 1, Oncogene Protein v-akt, Osteonectin, STAT3 Transcription Factor.
- chemical , pharmacology : Antineoplastic Agents, Phytogenic, Flavonoids.
- drug effects : Apoptosis, Cell Movement, Cell Proliferation, Cell Survival, Gene Expression Regulation, Neoplastic.
- drug therapy : Cerebellar Neoplasms, Medulloblastoma.
- genetics : Phosphatidylinositol 3-Kinases.
- metabolism : Phosphatidylinositol 3-Kinases.
- prevention & control : Neoplasm Invasiveness.
- Cell Line, Tumor, Humans.
Abstract
Icariin (ICA) is obtained from Epimedium brevicornu maxim and exploited to remedy miscellaneous cancers. But the role of ICA in medulloblastoma remains hazy. The research delved into the antitumor activity of ICA in medulloblastoma DAOY cells. ICA with diverse concentrations was utilized to stimulate DAOY cells, and the biological functions of ICA in medulloblastoma DAOY cells were examined. Then, the relative SPARC expression was determined in ICA-managed DAOY cells, and the pc-SPARC vector was transfected into DAOY cells to further probe the influence of SPARC and JAK1/STAT3 and PI3K/AKT pathways in ICA-managed DAOY cells. A xenograft model was established to investigate the function of ICA in vivo. ICA restrained cell viability, expedited apoptosis, prohibited cell migration and invasion, and meanwhile affected the associative factors expression in DAOY cells. Additionally, SPARC expression was declined in ICA-stimulated DAOY cells. Overexpressed SPARC reversed the functions of ICA in above-involved cell behaviors of DAYO cells and the correlative protein levels. Besides, ICA notably frustrated JAK1/STAT3 and PI3K/AKT activations in DAOY cells. Beyond that, ICA prohibited tumor formation in vivo. The results concluded that ICA exhibited the antitumor activity in DAOY cells via decreasing SPARC and inactivating JAK1/STAT3 and PI3K/AKT pathways.
DOI: 10.1002/ptr.6545
PubMed: 32011040
Affiliations:
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Yang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurosurgery, Jining No.1 People's Hospital, Jining, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Neurosurgery, Jining No.1 People's Hospital, Jining</wicri:regionArea><wicri:noRegion>Jining</wicri:noRegion></affiliation></author><author><name sortKey="Li, Guifang" sort="Li, Guifang" uniqKey="Li G" first="Guifang" last="Li">Guifang Li</name><affiliation wicri:level="1"><nlm:affiliation>Department of Occupational Medicine, Weifang People's Hospital, Weifang, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Occupational Medicine, Weifang People's Hospital, Weifang</wicri:regionArea><wicri:noRegion>Weifang</wicri:noRegion></affiliation></author></analytic><series><title level="j">Phytotherapy research : PTR</title><idno type="eISSN">1099-1573</idno><imprint><date when="2020" 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(génétique)</term><term>Phosphatidylinositol 3-kinases (métabolisme)</term><term>Prolifération cellulaire (effets des médicaments et des substances chimiques)</term><term>Protéine oncogène v-akt (génétique)</term><term>Protéine oncogène v-akt (métabolisme)</term><term>Régulation de l'expression des gènes tumoraux (effets des médicaments et des substances chimiques)</term><term>Survie cellulaire (effets des médicaments et des substances chimiques)</term><term>Tumeurs du cervelet (traitement médicamenteux)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Janus Kinase 1</term><term>Oncogene Protein v-akt</term><term>Osteonectin</term><term>STAT3 Transcription Factor</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Janus Kinase 1</term><term>Oncogene Protein v-akt</term><term>Osteonectin</term><term>STAT3 Transcription Factor</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Agents, Phytogenic</term><term>Flavonoids</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Cell Movement</term><term>Cell Proliferation</term><term>Cell Survival</term><term>Gene Expression Regulation, Neoplastic</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Cerebellar Neoplasms</term><term>Medulloblastoma</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Apoptose</term><term>Mouvement cellulaire</term><term>Prolifération cellulaire</term><term>Régulation de l'expression des gènes tumoraux</term><term>Survie cellulaire</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Phosphatidylinositol 3-Kinases</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteur de transcription STAT-3</term><term>Janus kinase 1</term><term>Ostéonectine</term><term>Phosphatidylinositol 3-kinases</term><term>Protéine oncogène v-akt</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Phosphatidylinositol 3-Kinases</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteur de transcription STAT-3</term><term>Janus kinase 1</term><term>Ostéonectine</term><term>Phosphatidylinositol 3-kinases</term><term>Protéine oncogène v-akt</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antinéoplasiques d'origine végétale</term><term>Flavonoïdes</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Neoplasm Invasiveness</term></keywords><keywords scheme="MESH" qualifier="prévention et contrôle" xml:lang="fr"><term>Invasion tumorale</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Médulloblastome</term><term>Tumeurs du cervelet</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Humains</term><term>Lignée cellulaire tumorale</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Icariin (ICA) is obtained from Epimedium brevicornu maxim and exploited to remedy miscellaneous cancers. But the role of ICA in medulloblastoma remains hazy. The research delved into the antitumor activity of ICA in medulloblastoma DAOY cells. ICA with diverse concentrations was utilized to stimulate DAOY cells, and the biological functions of ICA in medulloblastoma DAOY cells were examined. Then, the relative SPARC expression was determined in ICA-managed DAOY cells, and the pc-SPARC vector was transfected into DAOY cells to further probe the influence of SPARC and JAK1/STAT3 and PI3K/AKT pathways in ICA-managed DAOY cells. A xenograft model was established to investigate the function of ICA in vivo. ICA restrained cell viability, expedited apoptosis, prohibited cell migration and invasion, and meanwhile affected the associative factors expression in DAOY cells. Additionally, SPARC expression was declined in ICA-stimulated DAOY cells. Overexpressed SPARC reversed the functions of ICA in above-involved cell behaviors of DAYO cells and the correlative protein levels. Besides, ICA notably frustrated JAK1/STAT3 and PI3K/AKT activations in DAOY cells. Beyond that, ICA prohibited tumor formation in vivo. The results concluded that ICA exhibited the antitumor activity in DAOY cells via decreasing SPARC and inactivating JAK1/STAT3 and PI3K/AKT pathways.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" IndexingMethod="Curated" Owner="NLM"><PMID Version="1">32011040</PMID><DateCompleted><Year>2020</Year><Month>07</Month><Day>03</Day></DateCompleted><DateRevised><Year>2020</Year><Month>07</Month><Day>03</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1099-1573</ISSN><JournalIssue CitedMedium="Internet"><Volume>34</Volume><Issue>3</Issue><PubDate><Year>2020</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Phytotherapy research : PTR</Title><ISOAbbreviation>Phytother Res</ISOAbbreviation></Journal><ArticleTitle>Icariin inhibits proliferation, migration, and invasion of medulloblastoma DAOY cells by regulation of SPARC.</ArticleTitle><Pagination><MedlinePgn>591-600</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/ptr.6545</ELocationID><Abstract><AbstractText>Icariin (ICA) is obtained from Epimedium brevicornu maxim and exploited to remedy miscellaneous cancers. But the role of ICA in medulloblastoma remains hazy. The research delved into the antitumor activity of ICA in medulloblastoma DAOY cells. ICA with diverse concentrations was utilized to stimulate DAOY cells, and the biological functions of ICA in medulloblastoma DAOY cells were examined. Then, the relative SPARC expression was determined in ICA-managed DAOY cells, and the pc-SPARC vector was transfected into DAOY cells to further probe the influence of SPARC and JAK1/STAT3 and PI3K/AKT pathways in ICA-managed DAOY cells. A xenograft model was established to investigate the function of ICA in vivo. ICA restrained cell viability, expedited apoptosis, prohibited cell migration and invasion, and meanwhile affected the associative factors expression in DAOY cells. Additionally, SPARC expression was declined in ICA-stimulated DAOY cells. Overexpressed SPARC reversed the functions of ICA in above-involved cell behaviors of DAYO cells and the correlative protein levels. Besides, ICA notably frustrated JAK1/STAT3 and PI3K/AKT activations in DAOY cells. Beyond that, ICA prohibited tumor formation in vivo. The results concluded that ICA exhibited the antitumor activity in DAOY cells via decreasing SPARC and inactivating JAK1/STAT3 and PI3K/AKT pathways.</AbstractText><CopyrightInformation>© 2020 John Wiley & Sons, Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Yan</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Neurosurgery, Jining No.1 People's Hospital, Jining, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Guifang</ForeName><Initials>G</Initials><Identifier Source="ORCID">https://orcid.org/0000-0003-2908-3922</Identifier><AffiliationInfo><Affiliation>Department of Occupational Medicine, Weifang People's Hospital, Weifang, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>02</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Phytother Res</MedlineTA><NlmUniqueID>8904486</NlmUniqueID><ISSNLinking>0951-418X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000972">Antineoplastic Agents, Phytogenic</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005419">Flavonoids</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015676">Osteonectin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C577241">SPARC protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050796">STAT3 Transcription Factor</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C494086">STAT3 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.2</RegistryNumber><NameOfSubstance UI="C507904">JAK1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.2</RegistryNumber><NameOfSubstance UI="D053613">Janus Kinase 1</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D051058">Oncogene Protein v-akt</NameOfSubstance></Chemical><Chemical><RegistryNumber>VNM47R2QSQ</RegistryNumber><NameOfSubstance UI="C056599">icariin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000972" MajorTopicYN="N">Antineoplastic Agents, Phytogenic</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002465" MajorTopicYN="N">Cell Movement</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002528" MajorTopicYN="N">Cerebellar Neoplasms</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005419" MajorTopicYN="N">Flavonoids</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015972" MajorTopicYN="N">Gene Expression Regulation, Neoplastic</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053613" MajorTopicYN="N">Janus Kinase 1</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008527" MajorTopicYN="N">Medulloblastoma</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009361" MajorTopicYN="N">Neoplasm Invasiveness</DescriptorName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051058" MajorTopicYN="N">Oncogene Protein v-akt</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015676" MajorTopicYN="N">Osteonectin</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019869" MajorTopicYN="N">Phosphatidylinositol 3-Kinases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050796" MajorTopicYN="N">STAT3 Transcription Factor</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">JAK1/STAT3</Keyword><Keyword MajorTopicYN="N">PI3K/AKT</Keyword><Keyword MajorTopicYN="N">icariin</Keyword><Keyword MajorTopicYN="N">medulloblastoma</Keyword><Keyword MajorTopicYN="N">secreted protein acidic and rich in cysteine</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>05</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2019</Year><Month>09</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>10</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>2</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>7</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>2</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32011040</ArticleId><ArticleId IdType="doi">10.1002/ptr.6545</ArticleId></ArticleIdList><ReferenceList><Title>REFERENCES</Title><Reference><Citation>Ahir, B. K., Elias, N. M., & Lakka, S. S. (2017). SPARC overexpression alters microRNA expression profiles involved in tumor progression. Genes & Cancer, 8(1-2), 453-471. https://doi.org/10.18632/genesandcancer.130</Citation></Reference><Reference><Citation>Bhoopathi, P, Chetty, C, Gujrati, M, Dinh, DH, Rao, JS, Lakka, SS. 2010. SPARC stimulates neuronal differentiation of medulloblastoma cells via the IL-6/STAT3 pathway. Cancer Res 70(8): Abstract nr 2286.</Citation></Reference><Reference><Citation>Bhoopathi, P., Chetty, C., Gujrati, M., Rao, J., & Lakka, S. (2007). SPARC expression is associated with reduced angiogenesis in medulloblastoma. Cancer Res, 67, 3825-3825.</Citation></Reference><Reference><Citation>Brasme, J. F., Chalumeau, M., Doz, F., Lacour, B., Valteau-Couanet, D., Gaillard, S., … Grill, J. (2012). Interval between onset of symptoms and diagnosis of medulloblastoma in children: Distribution and determinants in a population-based study. Eur J Pediatr, 171(1), 25-32. https://doi.org/10.1007/s00431-011-1480-z</Citation></Reference><Reference><Citation>Chen, J., Wang, M., Xi, B., Xue, J., He, D., Zhang, J., & Zhao, Y. (2012). SPARC is a key regulator of proliferation, apoptosis and invasion in human ovarian cancer. PloS one, 7(8), e42413. https://doi.org/10.1371/journal.pone.0042413</Citation></Reference><Reference><Citation>Chen, K. M., Ge, B. F., Ma, H. P., Liu, X. Y., Bai, M. H., & Wang, Y. (2005). Icariin, a flavonoid from the herb Epimedium enhances the osteogenic differentiation of rat primary bone marrow stromal cells. Pharmazie, 60(12), 939-942.</Citation></Reference><Reference><Citation>Chetty, C., Dontula, R., Ganji, P. N., Gujrati, M., & Lakka, S. S. (2012). SPARC expression induces cell cycle arrest via STAT3 signaling pathway in medulloblastoma cells. Biochem Biophys Res Commun, 417(2), 874-879. https://doi.org/10.1016/j.bbrc.2011.12.065</Citation></Reference><Reference><Citation>Fan, C., Yang, Y., Liu, Y., Jiang, S., Di, S., Hu, W., et al. (2016). Icariin displays anticancer activity against human esophageal cancer cells via regulating endoplasmic reticulum stress-mediated apoptotic signaling. Sci Rep, 6, 21145.</Citation></Reference><Reference><Citation>Gui, Y., Zhang, J., Chen, L., Duan, S., Tang, J., Xu, W., et al. (2018). Icariin, a flavonoid with anti-cancer effects, alleviated paclitaxel-induced neuropathic pain in a SIRT1-dependent manner. Mol Pain, 14, 1744806918768970-1744806918768970.</Citation></Reference><Reference><Citation>Hartmann, W., Digon-Sontgerath, B., Koch, A., Waha, A., Endl, E., Dani, I., et al. (2006). Phosphatidylinositol 3'-kinase/AKT signaling is activated in medulloblastoma cell proliferation and is associated with reduced expression of PTEN. Clin Cancer Res, 12(10), 3019-3027. https://doi.org/10.1158/1078-0432.CCR-05-2187</Citation></Reference><Reference><Citation>Huang, S., Meng, N., Chang, B., Quan, X., Yuan, R., & Li, B. (2018). Anti-inflammatory activity of Epimedium brevicornu maxim ethanol extract. J Med Food, 21(7), 726-733. https://doi.org/10.1089/jmf.2017.4088</Citation></Reference><Reference><Citation>Khakban, A., Mohammadi, T., Lynd, L. D., Mabbott, D., Bouffet, E., Gastonguay, L., et al. (2017). Societal preferences in the treatment of pediatric medulloblastoma: Balancing risk of death and quality of life. Pediatr Blood Cancer, 64(6).</Citation></Reference><Reference><Citation>Li, J., Jiang, K., & Zhao, F. (2015). Icariin regulates the proliferation and apoptosis of human ovarian cancer cells through microRNA-21 by targeting PTEN, RECK and Bcl-2. Oncology reports, 33(6), 2829-2836. https://doi.org/10.3892/or.2015.3891</Citation></Reference><Reference><Citation>Li, S., Dong, P., Wang, J., Zhang, J., Gu, J., Wu, X., … Liu, Y. (2010). Icariin, a natural flavonol glycoside, induces apoptosis in human hepatoma SMMC-7721 cells via a ROS/JNK-dependent mitochondrial pathway. Cancer Lett, 298(2), 222-230. https://doi.org/10.1016/j.canlet.2010.07.009</Citation></Reference><Reference><Citation>Li, W. W., Gao, X. M., Wang, X. M., Guo, H., & Zhang, B. L. (2011). Icariin inhibits hydrogen peroxide-induced toxicity through inhibition of phosphorylation of JNK/p38 MAPK and p53 activity. Mutat Res, 708(1-2), 1-10. https://doi.org/10.1016/j.mrfmmm.2010.12.017</Citation></Reference><Reference><Citation>Livak, K. J., & Schmittgen, T. D. (2001). Analysis of relative gene expression data using real-time quantitative PCR and the 2−ΔΔCT method. Methods, 25(4), 402-408. https://doi.org/10.1006/meth.2001.1262</Citation></Reference><Reference><Citation>Lu, Y. F., Xu, Y. Y., Jin, F., Wu, Q., Shi, J. S., & Liu, J. (2014). Icariin is a PPARalpha activator inducing lipid metabolic gene expression in mice. Molecules (Basel, Switzerland), 19(11), 18179-18191.</Citation></Reference><Reference><Citation>Ma, H. P., Ming, L. G., Ge, B. F., Zhai, Y. K., Song, P., Xian, C. J., & Chen, K. M. (2011). Icariin is more potent than genistein in promoting osteoblast differentiation and mineralization in vitro. J Cell Biochem, 112(3), 916-923. https://doi.org/10.1002/jcb.23007</Citation></Reference><Reference><Citation>Ma, J., Gao, S., Xie, X., Sun, E., Zhang, M., Zhou, Q., et al. (2017). SPARC inhibits breast cancer bone metastasis and may be a clinical therapeutic target. Oncology letters, 14(5), 5876-5882.</Citation></Reference><Reference><Citation>Mao, S., He, M., Liu, G., Zhang, X., Li, Y., & Tang, L. (2013). Curcumin suppresses proliferation and induces apoptosis in human medulloblastoma cells via PI3k/Akt signaling pathway. Journal of Third Military Medical University, 35(6), 518-522.</Citation></Reference><Reference><Citation>Menekse, G., Gezercan, Y., Demirturk, P., Uysal, I., & Okten, A. I. (2015). Fatal cerebellar hemorrhage as an initial presentation of medulloblastoma in a child. J Pediatr Neurosci, 10(3), 287-289. https://doi.org/10.4103/1817-1745.165727</Citation></Reference><Reference><Citation>Polkinghorn, W. R., & Tarbell, N. J. (2007). Medulloblastoma: Tumorigenesis, current clinical paradigm, and efforts to improve risk stratification. Nature Clinical Practice Oncology, 4(5), 295-304. https://doi.org/10.1038/ncponc0794</Citation></Reference><Reference><Citation>Ramaswamy, V., Remke, M., Adamski, J., Bartels, U., Tabori, U., Wang, X., et al. (2016). Medulloblastoma subgroup-specific outcomes in irradiated children: Who are the true high-risk patients? Neuro Oncol, 18(2), 291-297.</Citation></Reference><Reference><Citation>Roussel, M. F., & Hatten, M. E. (2011). Cerebellum: Development and medulloblastoma. Curr Top Dev Biol, 94, 235-282. https://doi.org/10.1016/B978-0-12-380916-2.00008-5</Citation></Reference><Reference><Citation>Said, N., & Motamed, K. (2005). Absence of host-secreted protein acidic and rich in cysteine (SPARC) augments peritoneal ovarian carcinomatosis. Am J Pathol, 167(6), 1739-1752. https://doi.org/10.1016/S0002-9440(10)61255-2</Citation></Reference><Reference><Citation>Said, N., Najwer, I., & Motamed, K. (2007). Secreted protein acidic and rich in cysteine (SPARC) inhibits integrin-mediated adhesion and growth factor-dependent survival signaling in ovarian cancer. Am J Pathol, 170(3), 1054-1063.</Citation></Reference><Reference><Citation>Shi, D. B., Li, X. X., Zheng, H. T., Li, D. W., Cai, G. X., Peng, J. J., … Cai, S. J. (2014). Icariin-mediated inhibition of NF-kappaB activity enhances the in vitro and in vivo antitumour effect of 5-fluorouracil in colorectal cancer. Cell biochemistry and biophysics, 69(3), 523-530. https://doi.org/10.1007/s12013-014-9827-5</Citation></Reference><Reference><Citation>Sun, Y., Sun, X. H., Fan, W. J., Jiang, X. M., & Li, A. W. (2016). Icariin induces S-phase arrest and apoptosis in medulloblastoma cells. Cellular and molecular biology (Noisy-le-Grand, France), 62(4), 123-129.</Citation></Reference><Reference><Citation>Wang, L., Zhang, L., Chen, Z. B., Wu, J. Y., Zhang, X., & Xu, Y. (2009). Icariin enhances neuronal survival after oxygen and glucose deprivation by increasing SIRT1. Eur J Pharmacol, 609(1-3), 40-44. https://doi.org/10.1016/j.ejphar.2009.03.033</Citation></Reference><Reference><Citation>Wang, Y., Dong, H., Zhu, M., Ou, Y., Zhang, J., Luo, H., … Wei, L. (2010). Icariin exterts negative effects on human gastric cancer cell invasion and migration by vasodilator-stimulated phosphoprotein via Rac1 pathway. Eur J Pharmacol, 635(1-3), 40-48. https://doi.org/10.1016/j.ejphar.2010.03.017</Citation></Reference><Reference><Citation>Wu, Y. R., Qi, H. J., Deng, D. F., Luo, Y. Y., & Yang, S. L. (2016). MicroRNA-21 promotes cell proliferation, migration, and resistance to apoptosis through PTEN/PI3K/AKT signaling pathway in esophageal cancer. Tumour biology: The journal of the International Society for Oncodevelopmental Biology and Medicine, 37(9), 12061-12070. https://doi.org/10.1007/s13277-016-5074-2</Citation></Reference><Reference><Citation>Xiong, H, Zhang, ZG, Tian, XQ, Sun, DF, Liang, QC, Zhang, YJ, et al. 2008. Inhibition of JAK1, 2/STAT3 signaling induces apoptosis, cell cycle arrest, and reduces tumor cell invasion in colorectal cancer cells. Neoplasia (New York, N.Y.) 10(3): 287-297.</Citation></Reference><Reference><Citation>Xu, C. Q., Liu, B. J., Wu, J. F., Xu, Y. C., Duan, X. H., Cao, Y. X., & Dong, J. C. (2010). Icariin attenuates LPS-induced acute inflammatory responses: Involvement of PI3K/Akt and NF-kappaB signaling pathway. Eur J Pharmacol, 642(1-3), 146-153. https://doi.org/10.1016/j.ejphar.2010.05.012</Citation></Reference><Reference><Citation>Xu, Y, Li, Z, Yuan, L, Zhang, X, Lu, D, Huang, H, Wang Y 2013. Variation of epimedins A-C and icariin in ten representative populations of Epimedium brevicornu maxim., and implications for utilization. Chem Biodivers 10(4): 711-721, Variation of epimedins A - C and icariin in ten representative populations of Epimedium brevicornu Maxim., and implications for utilization, DOI: https://doi.org/10.1002/cbdv.201100424.</Citation></Reference><Reference><Citation>Yang, L., Wang, Y., Guo, H., & Guo, M. (2015). Synergistic anti-cancer effects of icariin and temozolomide in glioblastoma. Cell biochemistry and biophysics, 71(3), 1379-1385. https://doi.org/10.1007/s12013-014-0360-3</Citation></Reference><Reference><Citation>Ye, H. Y., & Lou, Y. J. (2005). Estrogenic effects of two derivatives of icariin on human breast cancer MCF-7 cells. Phytomedicine, 12(10), 735-741.</Citation></Reference><Reference><Citation>Zhang, B, Izadjoo, M, Horkayne-Szakaly, I, Morrison, A, Wear, DJ. 2011. Medulloblastoma and brucellosis-molecular evidence of Brucella sp in association with central nervous system cancer. Journal of Cancer 2: 136-141.</Citation></Reference><Reference><Citation>Zhang, D. C., Liu, J. L., Ding, Y. B., Xia, J. G., & Chen, G. Y. (2013). Icariin potentiates the antitumor activity of gemcitabine in gallbladder cancer by suppressing NF-κB. Acta Pharmacol Sin, 34(2), 301-308. https://doi.org/10.1038/aps.2012.162</Citation></Reference><Reference><Citation>Zhao, Y., Hou, Y., Tang, G., Cai, E., Liu, S., Yang, H., et al. (2014). Optimization of ultrasonic extraction of phenolic compounds from Epimedium brevicornum maxim using response surface methodology and evaluation of its antioxidant activities in vitro. J Anal Methods Chem, 2014, 864654.</Citation></Reference><Reference><Citation>ZHU, Dy, LOU, Yj. 2006. Icariin-mediated expression of cardiac genes and modulation of nitric oxide signaling pathway during differentiation of mouse embryonic stem cells into cardiomyocytes in vitro 1. Acta pharmacologica Sinica 27(3): 311-320, DOI: https://doi.org/10.1111/j.1745-7254.2006.00275.x.</Citation></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Yang, Yan" sort="Yang, Yan" uniqKey="Yang Y" first="Yan" last="Yang">Yan Yang</name></noRegion><name sortKey="Li, Guifang" sort="Li, Guifang" uniqKey="Li G" first="Guifang" last="Li">Guifang Li</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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