Please use this identifier to cite or link to this item: https://doi.org/10.3390/cancers12010211
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dc.titleSphingosine 1-phosphate receptor 2 induces otoprotective responses to cisplatin treatment
dc.contributor.authorWang, W.
dc.contributor.authorShanmugam, M.K.
dc.contributor.authorXiang, P.
dc.contributor.authorYam, T.Y.A.
dc.contributor.authorKumar, V.
dc.contributor.authorChew, W.S.
dc.contributor.authorChang, J.K.
dc.contributor.authorAli, M.Z.B.
dc.contributor.authorReolo, M.J.Y.
dc.contributor.authorPeh, Y.X.
dc.contributor.authorKarim, S.N.B.A.
dc.contributor.authorTan, A.Y.Y.
dc.contributor.authorSanda, T.
dc.contributor.authorSethi, G.
dc.contributor.authorHerr, D.R.
dc.date.accessioned2021-08-24T03:01:03Z
dc.date.available2021-08-24T03:01:03Z
dc.date.issued2020
dc.identifier.citationWang, W., Shanmugam, M.K., Xiang, P., Yam, T.Y.A., Kumar, V., Chew, W.S., Chang, J.K., Ali, M.Z.B., Reolo, M.J.Y., Peh, Y.X., Karim, S.N.B.A., Tan, A.Y.Y., Sanda, T., Sethi, G., Herr, D.R. (2020). Sphingosine 1-phosphate receptor 2 induces otoprotective responses to cisplatin treatment. Cancers 12 (1) : 211. ScholarBank@NUS Repository. https://doi.org/10.3390/cancers12010211
dc.identifier.issn2072-6694
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/199034
dc.description.abstractOtotoxicity is a major adverse effect of platinum-based chemotherapeutics and currently, there remains a lack of United States Food and Drug Administration-approved therapies to prevent or treat this problem. In our study, we examined the role of the sphingosine 1-phosphate receptor 2 (S1P2) in attenuating cisplatin-induced ototoxicity in several different animal models and cell lines. We found that ototoxicity in S1P2 knockout mice is dependent on reactive oxygen species (ROS) production and that S1P2 receptor activation with a specific agonist, CYM-5478, significantly attenuates cisplatin-induced defects, including hair cell degeneration in zebrafish and prolonged auditory brainstem response latency in rats. We also evaluated the cytoprotective effect of CYM-5478 across different cell lines and showed that CYM-5478 protects neural-derived cell lines but not breast cancer cells against cisplatin toxicity. We show that this selective protection of CYM-5478 is due to its differential effects on key regulators of apoptosis between neural cells and breast cancer cells. Overall, our study suggests that targeting the S1P2 receptor represents a promising therapeutic approach for the treatment of cisplatin-induced ototoxicity in cancer patients. © 2020 by the authors. Licensee MDPI, Basel, Switzerland.
dc.publisherMDPI AG
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceScopus OA2020
dc.subjectAcoustic startle response
dc.subjectAuditory brainstem response
dc.subjectCisplatin
dc.subjectCochlea
dc.subjectCYM-5478
dc.subjectHearing loss
dc.subjectOtotoxicity
dc.subjectReactive oxygen species
dc.subjectSphingosine 1-phosphate
dc.typeArticle
dc.contributor.departmentCANCER SCIENCE INSTITUTE OF SINGAPORE
dc.contributor.departmentDEAN'S OFFICE (DUKE-NUS MEDICAL SCHOOL)
dc.contributor.departmentDEPT OF MEDICINE
dc.contributor.departmentDEPT OF PAEDIATRICS
dc.contributor.departmentDEPT OF PHARMACOLOGY
dc.contributor.departmentDEPT OF PHYSIOLOGY
dc.description.doi10.3390/cancers12010211
dc.description.sourcetitleCancers
dc.description.volume12
dc.description.issue1
dc.description.page211
dc.published.statePublished
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