Please use this identifier to cite or link to this item: https://doi.org/10.26508/lsa.202101144
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dc.titleSuppression of isoprenylcysteine carboxylmethyltransferase compromises DNA damage repair
dc.contributor.authorTang, Jingyi
dc.contributor.authorCasey, Patrick J.
dc.contributor.authorWang, Mei
dc.date.accessioned2022-10-26T09:07:33Z
dc.date.available2022-10-26T09:07:33Z
dc.date.issued2021-10-05
dc.identifier.citationTang, Jingyi, Casey, Patrick J., Wang, Mei (2021-10-05). Suppression of isoprenylcysteine carboxylmethyltransferase compromises DNA damage repair. Life Science Alliance 4 (12) : e202101144. ScholarBank@NUS Repository. https://doi.org/10.26508/lsa.202101144
dc.identifier.issn2575-1077
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/233636
dc.description.abstractDNA damage is a double-edged sword for cancer cells. On the one hand, DNA damage–induced genomic instability contributes to cancer development; on the other hand, accumulating damage compromises proliferation and survival of cancer cells. Understanding the key regulators of DNA damage repair machinery would benefit the development of cancer therapies that induce DNA damage and apoptosis. In this study, we found that isoprenylcysteine carboxylmethyltransferase (ICMT), a posttranslational modification enzyme, plays an important role in DNA damage repair. We found that ICMT suppression consistently reduces the activity of MAPK signaling, which compromises the expression of key proteins in the DNA damage repair machinery. The ensuing accumulation of DNA damage leads to cell cycle arrest and apoptosis in multiple breast cancer cells. Interestingly, these observations are more pronounced in cells grown under anchorage-independent conditions or grown in vivo. Consistent with the negative impact on DNA repair, ICMT inhibition transforms the cancer cells into a “BRCA-like” state, hence sensitizing cancer cells to the treatment of PARP inhibitor and other DNA damage–inducing agents. © 2021 Tang et al.
dc.publisherRockefeller University Press
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.sourceScopus OA2021
dc.typeArticle
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.description.doi10.26508/lsa.202101144
dc.description.sourcetitleLife Science Alliance
dc.description.volume4
dc.description.issue12
dc.description.pagee202101144
dc.published.statePublished
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