Please use this identifier to cite or link to this item: https://doi.org/10.18632/oncotarget.1874
Title: SPHK1 regulates proliferation and survival responses in triplenegative breast cancer
Authors: Datta, 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 
Keywords: 2,2 dimethyl(1 oxo 2 hexadecyn 1 yl) 1,1 dimethylethyl ester 3 oxazolidinecarboxylic acid
docetaxel
doxorubicin
fluorouracil
mitogen activated protein kinase 1
mitogen activated protein kinase 3
phosphotransferase inhibitor
protein kinase B
ski 5c
small interfering RNA
sphingosine kinase 1
unclassified drug
phosphotransferase
sphingosine kinase
animal experiment
animal model
article
cancer growth
cancer prognosis
cancer survival
controlled study
drug sensitization
enzyme inhibition
female
gene silencing
human
human cell
human tissue
in vitro study
mouse
multiple cycle treatment
nonhuman
phase 2 clinical trial (topic)
regulatory mechanism
signal transduction
triple negative breast cancer
animal
cell proliferation
cell survival
enzymology
genetic transfection
genetics
MCF 7 cell line
metabolism
pathology
physiology
SCID mouse
triple negative breast cancer
tumor cell line
xenograft
Animals
Cell Line, Tumor
Cell Proliferation
Cell Survival
Female
Heterografts
Humans
MCF-7 Cells
Mice
Mice, SCID
Phosphotransferases (Alcohol Group Acceptor)
Transfection
Triple Negative Breast Neoplasms
Issue Date: 2014
Citation: Datta, 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
Abstract: Triple-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.
Source Title: Oncotarget
URI: https://scholarbank.nus.edu.sg/handle/10635/174167
ISSN: 19492553
DOI: 10.18632/oncotarget.1874
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