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Article: Elevated chemokine CC-motif receptor-like 2 (CCRL2) promotes cell migration and invasion in glioblastoma

TitleElevated chemokine CC-motif receptor-like 2 (CCRL2) promotes cell migration and invasion in glioblastoma
Authors
KeywordsCCRL2
Glioblastoma
Glioma dissemination
Tumor invasion
Tumor migration
Issue Date2012
Citation
Biochemical and Biophysical Research Communications, 2012, v. 429, n. 3-4, p. 168-172 How to Cite?
AbstractChemokine CC-motif receptor-like 2 (CCRL2) is a 7-transmembrane G protein-coupled receptor which plays a key role in lung dendritic cell trafficking to peripheral lymph nodes. The function and expression of CCRL2 in cancer is not understood at present. Here we report that CCRL2 expression level is elevated in human glioma patient samples and cell lines. The magnitude of increase is positively associated with increasing tumor grade, with the highest level observed in grade IV glioblastoma. By gain-of-function and loss-of-function studies, we further showed that CCRL2 did not regulate the growth of human glioblatoma U87 and U373 cells. Importantly, we demonstrated that over-expression of CCRL2 significantly enhanced the migration rate and invasiveness of the glioblastoma cells. Taken together, these results suggest for the first time that elevated CCRL2 in glioma promotes cell migration and invasion. The potential roles of CCRL2 as a novel therapeutic target and biomarker warrant further investigations. © 2012 Elsevier Inc.
Persistent Identifierhttp://hdl.handle.net/10722/325253
ISSN
2023 Impact Factor: 2.5
2023 SCImago Journal Rankings: 0.770
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYin, Fengqiong-
dc.contributor.authorXu, Zhenhua-
dc.contributor.authorWang, Zifeng-
dc.contributor.authorYao, Hong-
dc.contributor.authorShen, Zan-
dc.contributor.authorYu, Fang-
dc.contributor.authorTang, Yiping-
dc.contributor.authorFu, Dengli-
dc.contributor.authorLin, Sheng-
dc.contributor.authorLu, Gang-
dc.contributor.authorKung, Hsiang Fu-
dc.contributor.authorPoon, Wai Sang-
dc.contributor.authorHuang, Yunchao-
dc.contributor.authorLin, Marie Chia Mi-
dc.date.accessioned2023-02-27T07:30:59Z-
dc.date.available2023-02-27T07:30:59Z-
dc.date.issued2012-
dc.identifier.citationBiochemical and Biophysical Research Communications, 2012, v. 429, n. 3-4, p. 168-172-
dc.identifier.issn0006-291X-
dc.identifier.urihttp://hdl.handle.net/10722/325253-
dc.description.abstractChemokine CC-motif receptor-like 2 (CCRL2) is a 7-transmembrane G protein-coupled receptor which plays a key role in lung dendritic cell trafficking to peripheral lymph nodes. The function and expression of CCRL2 in cancer is not understood at present. Here we report that CCRL2 expression level is elevated in human glioma patient samples and cell lines. The magnitude of increase is positively associated with increasing tumor grade, with the highest level observed in grade IV glioblastoma. By gain-of-function and loss-of-function studies, we further showed that CCRL2 did not regulate the growth of human glioblatoma U87 and U373 cells. Importantly, we demonstrated that over-expression of CCRL2 significantly enhanced the migration rate and invasiveness of the glioblastoma cells. Taken together, these results suggest for the first time that elevated CCRL2 in glioma promotes cell migration and invasion. The potential roles of CCRL2 as a novel therapeutic target and biomarker warrant further investigations. © 2012 Elsevier Inc.-
dc.languageeng-
dc.relation.ispartofBiochemical and Biophysical Research Communications-
dc.subjectCCRL2-
dc.subjectGlioblastoma-
dc.subjectGlioma dissemination-
dc.subjectTumor invasion-
dc.subjectTumor migration-
dc.titleElevated chemokine CC-motif receptor-like 2 (CCRL2) promotes cell migration and invasion in glioblastoma-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.bbrc.2012.10.120-
dc.identifier.pmid23142225-
dc.identifier.scopuseid_2-s2.0-84870678232-
dc.identifier.volume429-
dc.identifier.issue3-4-
dc.identifier.spage168-
dc.identifier.epage172-
dc.identifier.eissn1090-2104-
dc.identifier.isiWOS:000312514200008-

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