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GPR110 promotes progression and metastasis of triple-negative breast cancer

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dc.contributor.authorNam, Hye-Jung-
dc.contributor.authorKim, Yeon-Ju-
dc.contributor.authorKang, Jae-Hyeok-
dc.contributor.authorLee, Su-Jae-
dc.date.accessioned2024-12-20T06:36:53Z-
dc.date.available2024-12-20T06:36:53Z-
dc.date.issued2022-05-
dc.identifier.issn2058-7716-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/203079-
dc.description.abstractBreast cancer is the most common type of cancer in women, and approximately 70% of all breast cancer patients use endocrine therapy, such as estrogen receptor modulators and aromatase inhibitors. In particular, triple-negative breast cancer (TNBC) remains a major threat due to the lack of targeted treatment options and poor clinical outcomes. Here, we found that GPR110 was highly expressed in TNBC and GPR110 plays a key role in TNBC progression by engaging the RAS signaling pathway (via G alpha s activation). High expression of GPR110 promoted EMT and CSC phenotypes in breast cancer. Consequently, our study highlights the critical role of GPR110 as a therapeutic target and inhibition of GPR110 could provide a therapeutic strategy for the treatment of TNBC patients.-
dc.format.extent8-
dc.language영어-
dc.language.isoENG-
dc.publisherSPRINGERNATURE-
dc.titleGPR110 promotes progression and metastasis of triple-negative breast cancer-
dc.typeArticle-
dc.publisher.location영국-
dc.identifier.doi10.1038/s41420-022-01053-x-
dc.identifier.wosid000800138200001-
dc.identifier.bibliographicCitationCELL DEATH DISCOVERY, v.8, no.1, pp 1 - 8-
dc.citation.titleCELL DEATH DISCOVERY-
dc.citation.volume8-
dc.citation.number1-
dc.citation.startPage1-
dc.citation.endPage8-
dc.type.docTypeArticle-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaCell Biology-
dc.relation.journalWebOfScienceCategoryCell Biology-
dc.subject.keywordPlusACTIVATION-
dc.identifier.urlhttps://www.nature.com/articles/s41420-022-01053-x-
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서울 자연과학대학 > 서울 생명과학과 > 1. Journal Articles

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