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Article: Loss of cytoskeleton protein ADD3 promotes tumor growth and angiogenesis in glioblastoma multiforme

TitleLoss of cytoskeleton protein ADD3 promotes tumor growth and angiogenesis in glioblastoma multiforme
Authors
KeywordsAdducin
Actin cytoskeleton
GBM
Vascular endothelial growth factor
Cell-matrix interaction
Issue Date2020
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canlet
Citation
Cancer Letters, 2020, v. 474, p. 118-126 How to Cite?
AbstractAdducin 3 (ADD3) is a crucial assembly factor in the actin cytoskeleton and has been found to be aberrantly expressed in various cancers, including glioblastoma multiforme (GBM). It has previously been studied in array-based studies with controversial findings as to its functional role in glioma. In microarray analyses of 452 glioma specimens, we found significant downregulation of ADD3 in GBM, but not in less malignant gliomas, compared to normal brain tissue, which suggests that its downregulation might underlie critical events during malignant progression. We also found that ADD3 was functionally dependent on cell-matrix interaction. In our in vivo study, the proliferative and angiogenic capacity of ADD3-depleted GBM cells was promoted, possibly through PCNA, while p53 and p21 expression was suppressed, and pro-angiogenic signals were induced through VEGF-VEGFR-2-mediated activation in endothelial cells. With correlative in vitro, in vivo, and clinical data, we provide compelling evidence on the putative tumor-suppressive role of ADD3 in modulating GBM growth and angiogenesis. As a preclinical study, our research offers a better understanding of the pathogenesis of glioma malignant progression for the benefit of future investigations.
Persistent Identifierhttp://hdl.handle.net/10722/280318
ISSN
2019 Impact Factor: 7.36
2015 SCImago Journal Rankings: 2.331

 

DC FieldValueLanguage
dc.contributor.authorKiang, MYK-
dc.contributor.authorZhang, P-
dc.contributor.authorLi, N-
dc.contributor.authorZHU, Z-
dc.contributor.authorJIN, L-
dc.contributor.authorLeung, GK-K-
dc.date.accessioned2020-02-07T07:39:26Z-
dc.date.available2020-02-07T07:39:26Z-
dc.date.issued2020-
dc.identifier.citationCancer Letters, 2020, v. 474, p. 118-126-
dc.identifier.issn0304-3835-
dc.identifier.urihttp://hdl.handle.net/10722/280318-
dc.description.abstractAdducin 3 (ADD3) is a crucial assembly factor in the actin cytoskeleton and has been found to be aberrantly expressed in various cancers, including glioblastoma multiforme (GBM). It has previously been studied in array-based studies with controversial findings as to its functional role in glioma. In microarray analyses of 452 glioma specimens, we found significant downregulation of ADD3 in GBM, but not in less malignant gliomas, compared to normal brain tissue, which suggests that its downregulation might underlie critical events during malignant progression. We also found that ADD3 was functionally dependent on cell-matrix interaction. In our in vivo study, the proliferative and angiogenic capacity of ADD3-depleted GBM cells was promoted, possibly through PCNA, while p53 and p21 expression was suppressed, and pro-angiogenic signals were induced through VEGF-VEGFR-2-mediated activation in endothelial cells. With correlative in vitro, in vivo, and clinical data, we provide compelling evidence on the putative tumor-suppressive role of ADD3 in modulating GBM growth and angiogenesis. As a preclinical study, our research offers a better understanding of the pathogenesis of glioma malignant progression for the benefit of future investigations.-
dc.languageeng-
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canlet-
dc.relation.ispartofCancer Letters-
dc.subjectAdducin-
dc.subjectActin cytoskeleton-
dc.subjectGBM-
dc.subjectVascular endothelial growth factor-
dc.subjectCell-matrix interaction-
dc.titleLoss of cytoskeleton protein ADD3 promotes tumor growth and angiogenesis in glioblastoma multiforme-
dc.typeArticle-
dc.identifier.emailKiang, MYK: mykiang@hku.hk-
dc.identifier.emailZhang, P: pingder@hku.hk-
dc.identifier.emailLeung, GK-K: gkkleung@hku.hk-
dc.identifier.authorityLeung, GK-K=rp00522-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.canlet.2020.01.007-
dc.identifier.pmid31958485-
dc.identifier.scopuseid_2-s2.0-85078114210-
dc.identifier.hkuros309133-
dc.identifier.volume474-
dc.identifier.spage118-
dc.identifier.epage126-
dc.publisher.placeIreland-

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