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Conference Paper: Targeting AXL in PIK3R2-amplified ovarian cancer

TitleTargeting AXL in PIK3R2-amplified ovarian cancer
Authors
Issue Date2020
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
Proceedings of the 111th Annual Meeting of the American Association for Cancer Research (AACR), Virtual Meeting, 27-28 April 2020; 22-24 June 2020. In Cancer Research, 2020, v. 80 n. 16, Suppl., Abstract 3052 How to Cite?
AbstractThe p85 regulatory subunit and its associated p110 catalytic subunit are components of the class IA PI3K that mediates the downstream signal of receptor tyrosine kinases. PIK3R2 (encoding p85β, one of the p85 isoforms) is commonly amplified in ovarian cancer patients. Importantly, high PIK3R2 expression significantly correlated with worse patient survival. Here, we showed that p85β promoted tumorigenic properties of ovarian cancer cells. The protein expression of a receptor tyrosine kinase AXL was positively regulated by p85β. AXL is a member of the TAM receptor family. The regulation was specific to AXL because the other two members (Tyro3 and MERTK) were not altered by p85β. Drug sensitivity assays suggested that inhibition of AXL reduced oncogenic activities of p85β in vitro and in vivo. Together, we propose p85β as a potential therapeutic target in ovarian cancer and therapeutic blockade of AXL signaling may be an effective strategy for ovarian cancer with PIK3R2 amplification.
Persistent Identifierhttp://hdl.handle.net/10722/287248
ISSN
2019 Impact Factor: 9.727
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorRao, L-
dc.contributor.authorMak, CY-
dc.contributor.authorZhou, Y-
dc.contributor.authorZhang, D-
dc.contributor.authorLi, X-
dc.contributor.authorLu, Y-
dc.contributor.authorMills, GB-
dc.contributor.authorCheung, WTL-
dc.date.accessioned2020-09-22T02:58:06Z-
dc.date.available2020-09-22T02:58:06Z-
dc.date.issued2020-
dc.identifier.citationProceedings of the 111th Annual Meeting of the American Association for Cancer Research (AACR), Virtual Meeting, 27-28 April 2020; 22-24 June 2020. In Cancer Research, 2020, v. 80 n. 16, Suppl., Abstract 3052-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/287248-
dc.description.abstractThe p85 regulatory subunit and its associated p110 catalytic subunit are components of the class IA PI3K that mediates the downstream signal of receptor tyrosine kinases. PIK3R2 (encoding p85β, one of the p85 isoforms) is commonly amplified in ovarian cancer patients. Importantly, high PIK3R2 expression significantly correlated with worse patient survival. Here, we showed that p85β promoted tumorigenic properties of ovarian cancer cells. The protein expression of a receptor tyrosine kinase AXL was positively regulated by p85β. AXL is a member of the TAM receptor family. The regulation was specific to AXL because the other two members (Tyro3 and MERTK) were not altered by p85β. Drug sensitivity assays suggested that inhibition of AXL reduced oncogenic activities of p85β in vitro and in vivo. Together, we propose p85β as a potential therapeutic target in ovarian cancer and therapeutic blockade of AXL signaling may be an effective strategy for ovarian cancer with PIK3R2 amplification.-
dc.languageeng-
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/-
dc.relation.ispartofCancer Research-
dc.relation.ispartofAmerican Association for Cancer Research Annual Meeting 2020-
dc.titleTargeting AXL in PIK3R2-amplified ovarian cancer-
dc.typeConference_Paper-
dc.identifier.emailMak, CY: vicmak8@hku.hk-
dc.identifier.emailZhou, Y: yzhou@hku.hk-
dc.identifier.emailCheung, WTL: lydiacwt@hku.hk-
dc.identifier.authorityCheung, WTL=rp02137-
dc.description.natureabstract-
dc.identifier.doi10.1158/1538-7445.AM2020-3052-
dc.identifier.hkuros314427-
dc.identifier.hkuros315989-
dc.identifier.volume80-
dc.identifier.issue16, Suppl.-
dc.identifier.spageAbstract 3052-
dc.identifier.epageAbstract 3052-
dc.publisher.placeUnited States-

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