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Article: Neoisoliquiritigenin inhibits tumor progression by targeting GRP78-β-catenin signaling in breast cancer

TitleNeoisoliquiritigenin inhibits tumor progression by targeting GRP78-β-catenin signaling in breast cancer
Authors
KeywordsNeoisoliquiritigenin
GRP78
β-catenin signaling
Breast cancer
Progression
Issue Date2017
PublisherBentham Science Publishers Ltd. The Journal's web site is located at http://www.bentham.org/ccdt/index.htm
Citation
Current Cancer Drug Targets, 2017, v. 18 n. 4, p. 390-399 How to Cite?
AbstractBackground: Breast cancer mortality has been stable or decreasing in the world, its incidence and recurrence rates have sharply risen worldwide in the recent years. Objective: To investigate the clinicopathological significance and potential function of GRP78 in the development and progression of breast cancer. To explore the effects of neoisoliquiritigenin (NISL) in breast cancer and the underlying mechanism. Method: GRP78 was detected by immunohistochemistry (IHC) using breast cancer tissue microarrays (TMAs), and the association between GRP78 levels and clinicopathological factors and prognosis was analyzed. The functional effects of GRP78 on breast cancer were validated by an MTT assay, foci formation assay, Matrigel invasion assay and mouse xenograft assay. The effects of NISL were tested by an MTT assay, apoptosis assay and mouse xenograft assay. A LigandFit algorithm, ATPase activity assay, western blot and IHC assay were used to discover the underlying mechanism of the effects of NSIL. Results: GRP78 was highly expressed in breast cancer cell lines and tissues. In addition, high expression of GRP78 was correlated to poor outcomes and distant metastasis. Functional experiments showed that GRP78 promoted breast cancer proliferation and invasion in vitro and in vivo. NISL inhibited cell proliferation and induced cell apoptosis in breast cancer by directly binding to GRP78 to regulate the β-catenin pathway. Conclusion: Taken together, these results highlighted the significance of GRP78 in breast cancer development and suggested NISL as a natural candidate to inhibit breast cancer by targeting GRP78 and β-catenin signaling.
Persistent Identifierhttp://hdl.handle.net/10722/248090
ISSN
2017 Impact Factor: 2.626
2015 SCImago Journal Rankings: 1.537
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorTang, H-
dc.contributor.authorPeng, F-
dc.contributor.authorHuang, X-
dc.contributor.authorXie, X-
dc.contributor.authorChen, B-
dc.contributor.authorShen, J-
dc.contributor.authorGao, F-
dc.contributor.authorYou, J-
dc.contributor.authorChen, J-
dc.date.accessioned2017-10-18T08:37:39Z-
dc.date.available2017-10-18T08:37:39Z-
dc.date.issued2017-
dc.identifier.citationCurrent Cancer Drug Targets, 2017, v. 18 n. 4, p. 390-399-
dc.identifier.issn1568-0096-
dc.identifier.urihttp://hdl.handle.net/10722/248090-
dc.description.abstractBackground: Breast cancer mortality has been stable or decreasing in the world, its incidence and recurrence rates have sharply risen worldwide in the recent years. Objective: To investigate the clinicopathological significance and potential function of GRP78 in the development and progression of breast cancer. To explore the effects of neoisoliquiritigenin (NISL) in breast cancer and the underlying mechanism. Method: GRP78 was detected by immunohistochemistry (IHC) using breast cancer tissue microarrays (TMAs), and the association between GRP78 levels and clinicopathological factors and prognosis was analyzed. The functional effects of GRP78 on breast cancer were validated by an MTT assay, foci formation assay, Matrigel invasion assay and mouse xenograft assay. The effects of NISL were tested by an MTT assay, apoptosis assay and mouse xenograft assay. A LigandFit algorithm, ATPase activity assay, western blot and IHC assay were used to discover the underlying mechanism of the effects of NSIL. Results: GRP78 was highly expressed in breast cancer cell lines and tissues. In addition, high expression of GRP78 was correlated to poor outcomes and distant metastasis. Functional experiments showed that GRP78 promoted breast cancer proliferation and invasion in vitro and in vivo. NISL inhibited cell proliferation and induced cell apoptosis in breast cancer by directly binding to GRP78 to regulate the β-catenin pathway. Conclusion: Taken together, these results highlighted the significance of GRP78 in breast cancer development and suggested NISL as a natural candidate to inhibit breast cancer by targeting GRP78 and β-catenin signaling.-
dc.languageeng-
dc.publisherBentham Science Publishers Ltd. The Journal's web site is located at http://www.bentham.org/ccdt/index.htm-
dc.relation.ispartofCurrent Cancer Drug Targets-
dc.subjectNeoisoliquiritigenin-
dc.subjectGRP78-
dc.subjectβ-catenin signaling-
dc.subjectBreast cancer-
dc.subjectProgression-
dc.titleNeoisoliquiritigenin inhibits tumor progression by targeting GRP78-β-catenin signaling in breast cancer-
dc.typeArticle-
dc.identifier.emailTang, H: tanghl3@hku.hk-
dc.identifier.emailShen, J: shenjg@hku.hk-
dc.identifier.emailChen, J: abchen@hkucc.hku.hk-
dc.identifier.authorityShen, J=rp00487-
dc.identifier.authorityChen, J=rp01316-
dc.identifier.doi10.2174/1568009617666170914155355-
dc.identifier.pmid28914191-
dc.identifier.scopuseid_2-s2.0-85046793254-
dc.identifier.hkuros279758-
dc.identifier.volume18-
dc.identifier.issue4-
dc.identifier.spage390-
dc.identifier.epage399-
dc.identifier.isiWOS:000430264200009-
dc.publisher.placeNetherlands-

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