Please use this identifier to cite or link to this item: https://doi.org/10.18632/oncotarget.1874
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dc.titleSPHK1 regulates proliferation and survival responses in triplenegative breast cancer
dc.contributor.authorDatta, A
dc.contributor.authorLoo, S.Y
dc.contributor.authorHuang, B
dc.contributor.authorWong, L
dc.contributor.authorTan, S.S.L
dc.contributor.authorTan, T.Z
dc.contributor.authorLee, S.-C
dc.contributor.authorThiery, J.P
dc.contributor.authorLim, Y.C
dc.contributor.authorYong, W.P
dc.contributor.authorLam, Y
dc.contributor.authorKumar, A.P
dc.contributor.authorYap, C.T
dc.date.accessioned2020-09-03T10:41:59Z
dc.date.available2020-09-03T10:41:59Z
dc.date.issued2014
dc.identifier.citationDatta, A, Loo, S.Y, Huang, B, Wong, L, Tan, S.S.L, Tan, T.Z, Lee, S.-C, Thiery, J.P, Lim, Y.C, Yong, W.P, Lam, Y, Kumar, A.P, Yap, C.T (2014). SPHK1 regulates proliferation and survival responses in triplenegative breast cancer. Oncotarget 5 (15) : 5920-5933. ScholarBank@NUS Repository. https://doi.org/10.18632/oncotarget.1874
dc.identifier.issn19492553
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/174167
dc.description.abstractTriple-negative breast cancer (TNBC) is characterized by unique aggressive behavior and lack of targeted therapies. Among the various molecular subtypes of breast cancer, it was observed that TNBCs express elevated levels of sphingosine kinase 1 (SPHK1) compared to other breast tumor subtypes. High levels of SPHK1 gene expression correlated with poor overall and progression- free survival, as well as poor response to Doxorubicin-based treatment. Inhibition of SPHK1 was found to attenuate ERK1/2 and AKT signaling and reduce growth of TNBC cells in vitro and in a xenograft SCID mouse model. Moreover, SPHK1 inhibition by siRNA knockdown or treatment with SKI-5C sensitizes TNBCs to chemotherapeutic drugs. Our findings suggest that SPHK1 inhibition, which effectively counteracts oncogenic signaling through ERK1/2 and AKT pathways, is a potentially important anti-tumor strategy in TNBC. A combination of SPHK1 inhibitors with chemotherapeutic agents may be effective against this aggressive subtype of breast cancer.
dc.sourceUnpaywall 20200831
dc.subject2,2 dimethyl(1 oxo 2 hexadecyn 1 yl) 1,1 dimethylethyl ester 3 oxazolidinecarboxylic acid
dc.subjectdocetaxel
dc.subjectdoxorubicin
dc.subjectfluorouracil
dc.subjectmitogen activated protein kinase 1
dc.subjectmitogen activated protein kinase 3
dc.subjectphosphotransferase inhibitor
dc.subjectprotein kinase B
dc.subjectski 5c
dc.subjectsmall interfering RNA
dc.subjectsphingosine kinase 1
dc.subjectunclassified drug
dc.subjectphosphotransferase
dc.subjectsphingosine kinase
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectarticle
dc.subjectcancer growth
dc.subjectcancer prognosis
dc.subjectcancer survival
dc.subjectcontrolled study
dc.subjectdrug sensitization
dc.subjectenzyme inhibition
dc.subjectfemale
dc.subjectgene silencing
dc.subjecthuman
dc.subjecthuman cell
dc.subjecthuman tissue
dc.subjectin vitro study
dc.subjectmouse
dc.subjectmultiple cycle treatment
dc.subjectnonhuman
dc.subjectphase 2 clinical trial (topic)
dc.subjectregulatory mechanism
dc.subjectsignal transduction
dc.subjecttriple negative breast cancer
dc.subjectanimal
dc.subjectcell proliferation
dc.subjectcell survival
dc.subjectenzymology
dc.subjectgenetic transfection
dc.subjectgenetics
dc.subjectMCF 7 cell line
dc.subjectmetabolism
dc.subjectpathology
dc.subjectphysiology
dc.subjectSCID mouse
dc.subjecttriple negative breast cancer
dc.subjecttumor cell line
dc.subjectxenograft
dc.subjectAnimals
dc.subjectCell Line, Tumor
dc.subjectCell Proliferation
dc.subjectCell Survival
dc.subjectFemale
dc.subjectHeterografts
dc.subjectHumans
dc.subjectMCF-7 Cells
dc.subjectMice
dc.subjectMice, SCID
dc.subjectPhosphotransferases (Alcohol Group Acceptor)
dc.subjectTransfection
dc.subjectTriple Negative Breast Neoplasms
dc.typeArticle
dc.contributor.departmentDEPT OF PHYSIOLOGY
dc.contributor.departmentDEPT OF CHEMISTRY
dc.contributor.departmentCANCER SCIENCE INSTITUTE OF SINGAPORE
dc.contributor.departmentDEPT OF MEDICINE
dc.contributor.departmentDEPT OF BIOCHEMISTRY
dc.contributor.departmentDEPT OF PATHOLOGY
dc.contributor.departmentDEPT OF PHARMACOLOGY
dc.description.doi10.18632/oncotarget.1874
dc.description.sourcetitleOncotarget
dc.description.volume5
dc.description.issue15
dc.description.page5920-5933
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