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Article: Induction of apoptosis in glioma cells by molecules released from activated macrophages

TitleInduction of apoptosis in glioma cells by molecules released from activated macrophages
Authors
KeywordsApoptosis
Glioma
Interferon gamma
Macrophage
Tumor necrosis factor alpha
Issue Date2002
Citation
Journal of Neuro-Oncology, 2002, v. 57, n. 3, p. 179-186 How to Cite?
AbstractMacrophages play an important role in the regulation of malignant tumors. Although glioma contains abundance of macrophages, their role in apoptosis of glioma is not known. We stimulated macrophages with lipopolysaccharide and culture supernatants of activated macrophages were collected to treat glioma cells. The results showed that molecules released from activated macrophages significantly increased apoptosis of glioma via Fas/FasL and caspase-3 pathways. The level of soluble Fas did not appear to be involved in the mechanism responsible for apoptosis seen in this study, as its level was barely detected in both experimental and control groups. Two cytokines, TNFα and IFNγ, were significantly elevated in the supernatant obtained from the activated macrophages. Considering an important role of these two molecules in the induction of apoptosis mediated by the Fas/FasL system, the present data suggested that TNFα and IFNγ were the main molecules to trigger the cascade of apoptotic reactions in glioma cells. In conclusion, the present study indicates that molecules released from the activated macrophages provide significant signals to stimulate the expression of Fas/FasL and caspase-3, which function to induce apoptosis in glioma cells.
Persistent Identifierhttp://hdl.handle.net/10722/324934
ISSN
2023 Impact Factor: 3.2
2023 SCImago Journal Rankings: 1.131
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChen, George G.-
dc.contributor.authorChun, Ying S.-
dc.contributor.authorChak, Ernest C.W.-
dc.contributor.authorLeung, Billy C.S.-
dc.contributor.authorPoon, Wai S.-
dc.date.accessioned2023-02-27T07:28:22Z-
dc.date.available2023-02-27T07:28:22Z-
dc.date.issued2002-
dc.identifier.citationJournal of Neuro-Oncology, 2002, v. 57, n. 3, p. 179-186-
dc.identifier.issn0167-594X-
dc.identifier.urihttp://hdl.handle.net/10722/324934-
dc.description.abstractMacrophages play an important role in the regulation of malignant tumors. Although glioma contains abundance of macrophages, their role in apoptosis of glioma is not known. We stimulated macrophages with lipopolysaccharide and culture supernatants of activated macrophages were collected to treat glioma cells. The results showed that molecules released from activated macrophages significantly increased apoptosis of glioma via Fas/FasL and caspase-3 pathways. The level of soluble Fas did not appear to be involved in the mechanism responsible for apoptosis seen in this study, as its level was barely detected in both experimental and control groups. Two cytokines, TNFα and IFNγ, were significantly elevated in the supernatant obtained from the activated macrophages. Considering an important role of these two molecules in the induction of apoptosis mediated by the Fas/FasL system, the present data suggested that TNFα and IFNγ were the main molecules to trigger the cascade of apoptotic reactions in glioma cells. In conclusion, the present study indicates that molecules released from the activated macrophages provide significant signals to stimulate the expression of Fas/FasL and caspase-3, which function to induce apoptosis in glioma cells.-
dc.languageeng-
dc.relation.ispartofJournal of Neuro-Oncology-
dc.subjectApoptosis-
dc.subjectGlioma-
dc.subjectInterferon gamma-
dc.subjectMacrophage-
dc.subjectTumor necrosis factor alpha-
dc.titleInduction of apoptosis in glioma cells by molecules released from activated macrophages-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1023/A:1015763916020-
dc.identifier.pmid12125980-
dc.identifier.scopuseid_2-s2.0-0036560009-
dc.identifier.volume57-
dc.identifier.issue3-
dc.identifier.spage179-
dc.identifier.epage186-
dc.identifier.isiWOS:000176734500002-

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