Detailed Information

Cited 0 time in webofscience Cited 16 time in scopus
Metadata Downloads

TC Mps1 12, a novel Mps1 inhibitor, suppresses the growth of hepatocellular carcinoma cells via the accumulation of chromosomal instability

Full metadata record
DC Field Value Language
dc.contributor.authorChoi, Minji-
dc.contributor.authorMin, Yoo Hong-
dc.contributor.authorPyo, Jaehyuk-
dc.contributor.authorLee, Chang-Woo-
dc.contributor.authorJang, Chang-Young-
dc.contributor.authorKim, Ja-Eun-
dc.date.available2021-02-22T11:13:10Z-
dc.date.issued2017-06-
dc.identifier.issn0007-1188-
dc.identifier.issn1476-5381-
dc.identifier.urihttps://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/8290-
dc.description.abstractBackground and PurposeChromosomal instability is not only a hallmark of cancer but also an attractive therapeutic target. A diverse set of mitotic kinases maintains chromosomal stability. One of these is monopolar spindle 1 (Mps1, also known as TTK), which is essential for chromosome alignment and for the spindle assembly checkpoint (SAC). Pharmacological inhibition of Mps1 has been suggested as a cancer therapeutic; however, despite the existence of a novel Mps1 inhibitor, TC Mps1 12, no such studies have been performed. Experimental ApproachThe effects of TC Mps1 12 on cell viability, chromosome alignment, centrosome number, mitotic duration, apoptosis and SAC were determined in hepatocellular carcinoma (HCC) cells. In addition, the association of Mps1 expression with the overall survival of HCC patients was analysed. Key ResultsTreatment of human HCC cells with TC Mps1 12 led to chromosome misalignment and missegregation, and disorganization of centrosomes. Even in the presence of these errors, TC Mps1 12-treated cells overrode the SAC, resulting in a shortened mitotic duration and mitotic slippage. This mitotic catastrophe triggered apoptosis and, finally, inhibited the growth of HCC cells. In addition, the expression of the Mps1-encoding TTK gene was associated with poor overall survival of HCC patients. Conclusion and ImplicationsTC Mps1 12 results in the accumulation of chromosomal instabilities and mitotic catastrophe in HCC cells. Overall, these data demonstrate that the inhibition of Mps1 kinase using TC Mps1 12 is a promising therapeutic approach for liver cancer.-
dc.format.extent16-
dc.language영어-
dc.language.isoENG-
dc.publisherWILEY-
dc.titleTC Mps1 12, a novel Mps1 inhibitor, suppresses the growth of hepatocellular carcinoma cells via the accumulation of chromosomal instability-
dc.typeArticle-
dc.publisher.location미국-
dc.identifier.doi10.1111/bph.13782-
dc.identifier.scopusid2-s2.0-85018660029-
dc.identifier.wosid000402143300019-
dc.identifier.bibliographicCitationBRITISH JOURNAL OF PHARMACOLOGY, v.174, no.12, pp 1810 - 1825-
dc.citation.titleBRITISH JOURNAL OF PHARMACOLOGY-
dc.citation.volume174-
dc.citation.number12-
dc.citation.startPage1810-
dc.citation.endPage1825-
dc.type.docTypeArticle-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClasssci-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaPharmacology & Pharmacy-
dc.relation.journalWebOfScienceCategoryPharmacology & Pharmacy-
dc.subject.keywordPlusSPINDLE ASSEMBLY CHECKPOINT-
dc.subject.keywordPlusSPECIFICITY PROTEIN-KINASE-
dc.subject.keywordPlusP53-DEFICIENT CANCER-CELLS-
dc.subject.keywordPlusSMALL-MOLECULE INHIBITOR-
dc.subject.keywordPlusPOLE BODY DUPLICATION-
dc.subject.keywordPlusMITOTIC CHECKPOINT-
dc.subject.keywordPlusAURORA-B-
dc.subject.keywordPlusTARGETING MPS1-
dc.subject.keywordPlusCONCISE GUIDE-
dc.subject.keywordPlusTTK-
dc.identifier.urlhttps://bpspubs.onlinelibrary.wiley.com/doi/full/10.1111/bph.13782-
Files in This Item
Go to Link
Appears in
Collections
약학대학 > 약학부 > 1. Journal Articles

qrcode

Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.

Related Researcher

Researcher Jang, Chang Young photo

Jang, Chang Young
약학대학 (약학부)
Read more

Altmetrics

Total Views & Downloads

BROWSE