File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Tetraploidization increases sensitivity to Aurora B kinase inhibition

TitleTetraploidization increases sensitivity to Aurora B kinase inhibition
Authors
KeywordsAurora kinases
Tetraploidy
Cell cycle
Mitosis
Cancer
Issue Date2012
Citation
Cell Cycle, 2012, v. 11, n. 13, p. 2567-2577 How to Cite?
AbstractAurora kinases are overexpressed in many cancers and are targets for anticancer drugs. The yeast homolog of Aurora B kinase, IPL1, was found to be a ploidy-specific lethality gene. Given that polyploidization is a common feature of many cancers, we hypothesized polyploidization also sensitizes mammalian cells to inhibition of Aurora kinases. Using two models of apparent diploid vs. tetraploid cell lines (one based on the hepatocellular carcinoma cell line Hep3B and another on untransformed mouse fibroblasts), we found that tetraploid cells were more sensitive to Aurora B inhibition than their diploid counterparts. Apoptosis could be induced in tetraploid cells by two different Aurora B inhibitors. Furthermore, tetraploid cells were sensitive to Aurora B inhibition but were not affected by Aurora A inhibition. Interestingly, the underlying mechanism was due to mitotic slippage and the subsequent excessive genome reduplication. In support of this, abolition of cytokinesis with dihydrocytochalasin B resulted in similar effects on tetraploid cells as Aurora B inhibition. These results indicate that inhibition of Aurora B or cytokinesis can promote apoptosis effectively in polyploid cancer cells. © 2012 Landes Bioscience.
Persistent Identifierhttp://hdl.handle.net/10722/307124
ISSN
2023 Impact Factor: 3.4
2023 SCImago Journal Rankings: 0.947
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMarxer, Miriam-
dc.contributor.authorFoucar, Charles E.-
dc.contributor.authorMan, Wing Yu-
dc.contributor.authorChen, Yu-
dc.contributor.authorMa, Hoi Tang-
dc.contributor.authorPoon, Randy Y.C.-
dc.date.accessioned2021-11-03T06:21:59Z-
dc.date.available2021-11-03T06:21:59Z-
dc.date.issued2012-
dc.identifier.citationCell Cycle, 2012, v. 11, n. 13, p. 2567-2577-
dc.identifier.issn1538-4101-
dc.identifier.urihttp://hdl.handle.net/10722/307124-
dc.description.abstractAurora kinases are overexpressed in many cancers and are targets for anticancer drugs. The yeast homolog of Aurora B kinase, IPL1, was found to be a ploidy-specific lethality gene. Given that polyploidization is a common feature of many cancers, we hypothesized polyploidization also sensitizes mammalian cells to inhibition of Aurora kinases. Using two models of apparent diploid vs. tetraploid cell lines (one based on the hepatocellular carcinoma cell line Hep3B and another on untransformed mouse fibroblasts), we found that tetraploid cells were more sensitive to Aurora B inhibition than their diploid counterparts. Apoptosis could be induced in tetraploid cells by two different Aurora B inhibitors. Furthermore, tetraploid cells were sensitive to Aurora B inhibition but were not affected by Aurora A inhibition. Interestingly, the underlying mechanism was due to mitotic slippage and the subsequent excessive genome reduplication. In support of this, abolition of cytokinesis with dihydrocytochalasin B resulted in similar effects on tetraploid cells as Aurora B inhibition. These results indicate that inhibition of Aurora B or cytokinesis can promote apoptosis effectively in polyploid cancer cells. © 2012 Landes Bioscience.-
dc.languageeng-
dc.relation.ispartofCell Cycle-
dc.subjectAurora kinases-
dc.subjectTetraploidy-
dc.subjectCell cycle-
dc.subjectMitosis-
dc.subjectCancer-
dc.titleTetraploidization increases sensitivity to Aurora B kinase inhibition-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.4161/cc.20947-
dc.identifier.pmid22722494-
dc.identifier.scopuseid_2-s2.0-84863787422-
dc.identifier.volume11-
dc.identifier.issue13-
dc.identifier.spage2567-
dc.identifier.epage2577-
dc.identifier.eissn1551-4005-
dc.identifier.isiWOS:000306088600025-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats