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2016 ; 9
(ä): 3473-84
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Function of AURKA protein kinase in the formation of vasculogenic mimicry in
triple-negative breast cancer stem cells
#MMPMID27366084
Liu Y
; Sun B
; Liu T
; Zhao X
; Wang X
; Li Y
; Meng J
; Gu Q
; Liu F
; Dong X
; Liu P
; Sun R
; Zhao N
Onco Targets Ther
2016[]; 9
(ä): 3473-84
PMID27366084
show ga
Tumor cell vasculogenic mimicry (VM), a newly defined pattern of tumor blood
supply, signifies the functional plasticity of aggressive cancer cells forming
vascular networks. VM and cancer stem cells (CSCs) have been shown to be
associated with tumor growth, local invasion, and distant metastasis. In our
previous study, CSCs in triple-negative breast cancer were potential to
participate in VM formation. In this study, breast CSCs were isolated from the
triple-negative breast cancer cell line MDA-MB-231 by using mammosphere culture.
Western blotting and reverse transcription polymerase chain reaction showed that
mammosphere cells displayed an increased expression of AURKA protein kinase and
stem cell marker c-myc and sox2. The VM formation by mammosphere cells was
inhibited by AURKA knockdown or the addition of AURKA inhibitor MLN8237. In the
meantime, MLN8237 induced the increased E-cadherin and decreased c-myc, sox2, and
?-catenin expressions. The function of AURKA in VM formation was further
confirmed using a xenograft-murine model. The results suggested that AURKA
protein kinase is involved in VM formation of CSCs and may become a new treatment
target in suppressing VM and metastasis of breast cancer.