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Article: A natural product-like JAK2/STAT3 inhibitor induces apoptosis of malignant melanoma cells

TitleA natural product-like JAK2/STAT3 inhibitor induces apoptosis of malignant melanoma cells
Authors
Issue Date2017
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
PLoS One, 2017, v. 12, p. e0177123:1-12 How to Cite?
AbstractThe JAK2/STAT3 signaling pathway plays a critical role in tumorigenesis, and has been suggested as a potential molecular target for anti-melanoma therapeutics. However, few JAK2 inhibitors were being tested for melanoma therapy. In this study, eight amentoflavone analogues were evaluated for their activity against human malignant melanoma cells. The most potent analogue, compound 1, inhibited the phosphorylation of JAK2 and STAT3 in human melanoma cells, but had no discernible effect on total JAK2 and STAT3 levels. A cellular thermal shift assay was performed to identify that JAK2 is engaged by 1 in cell lysates. Moreover, compound 1 showed higher antiproliferative activity against human melanoma A375 cells compared to a panel of cancer and normal cell lines. Compound 1 also activated caspase-3 and cleaved PARP, which are markers of apoptosis, and suppressed the anti-apoptotic Bcl-2 level. Finally, compound 1 induced apoptosis in 80% of treated melanoma cells. To our knowledge, compound 1 is the first amentoflavone-based JAK2 inhibitor to be investigated for use as an anti-melanoma agent.
Persistent Identifierhttp://hdl.handle.net/10722/243006
ISSN
2019 Impact Factor: 2.74
2015 SCImago Journal Rankings: 1.395
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWu, KJ-
dc.contributor.authorHuang, JM-
dc.contributor.authorZhong, HJ-
dc.contributor.authorDong, ZZ-
dc.contributor.authorVellaisamy, K-
dc.contributor.authorLu, JJ-
dc.contributor.authorChen, XP-
dc.contributor.authorChiu, P-
dc.contributor.authorKwong, DWJ-
dc.contributor.authorHan, QB-
dc.contributor.authorMa, DL-
dc.contributor.authorLeung, CH-
dc.date.accessioned2017-08-25T02:48:38Z-
dc.date.available2017-08-25T02:48:38Z-
dc.date.issued2017-
dc.identifier.citationPLoS One, 2017, v. 12, p. e0177123:1-12-
dc.identifier.issn1932-6203-
dc.identifier.urihttp://hdl.handle.net/10722/243006-
dc.description.abstractThe JAK2/STAT3 signaling pathway plays a critical role in tumorigenesis, and has been suggested as a potential molecular target for anti-melanoma therapeutics. However, few JAK2 inhibitors were being tested for melanoma therapy. In this study, eight amentoflavone analogues were evaluated for their activity against human malignant melanoma cells. The most potent analogue, compound 1, inhibited the phosphorylation of JAK2 and STAT3 in human melanoma cells, but had no discernible effect on total JAK2 and STAT3 levels. A cellular thermal shift assay was performed to identify that JAK2 is engaged by 1 in cell lysates. Moreover, compound 1 showed higher antiproliferative activity against human melanoma A375 cells compared to a panel of cancer and normal cell lines. Compound 1 also activated caspase-3 and cleaved PARP, which are markers of apoptosis, and suppressed the anti-apoptotic Bcl-2 level. Finally, compound 1 induced apoptosis in 80% of treated melanoma cells. To our knowledge, compound 1 is the first amentoflavone-based JAK2 inhibitor to be investigated for use as an anti-melanoma agent.-
dc.languageeng-
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action-
dc.relation.ispartofPLoS One-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleA natural product-like JAK2/STAT3 inhibitor induces apoptosis of malignant melanoma cells-
dc.typeArticle-
dc.identifier.emailChiu, P: pchiu@hku.hk-
dc.identifier.authorityChiu, P=rp00680-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pone.0177123-
dc.identifier.hkuros274434-
dc.identifier.volume12-
dc.identifier.spagee0177123:1-
dc.identifier.epage12-
dc.identifier.isiWOS:000402611800006-
dc.publisher.placeUnited States-

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