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2017 ; 8
(18
): 30252-30264
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English Wikipedia
Aspirin regulation of c-myc and cyclinD1 proteins to overcome tamoxifen
resistance in estrogen receptor-positive breast cancer cells
#MMPMID28415819
Cheng R
; Liu YJ
; Cui JW
; Yang M
; Liu XL
; Li P
; Wang Z
; Zhu LZ
; Lu SY
; Zou L
; Wu XQ
; Li YX
; Zhou Y
; Fang ZY
; Wei W
Oncotarget
2017[May]; 8
(18
): 30252-30264
PMID28415819
show ga
Tamoxifen is still the most commonly used endocrine therapy drug for estrogen
receptor (ER)-positive breast cancer patients and has an excellent outcome, but
tamoxifen resistance remains a great impediment to successful treatment. Recent
studies have prompted an anti-tumor effect of aspirin. Here, we demonstrated that
aspirin not only inhibits the growth of ER-positive breast cancer cell line
MCF-7, especially when combined with tamoxifen, but also has a potential function
to overcome tamoxifen resistance in MCF-7/TAM. Aspirin combined with tamoxifen
can down regulate cyclinD1 and block cell cycle in G0/G1 phase. Besides,
tamoxifen alone represses c-myc, progesterone receptor (PR) and cyclinD1 in MCF-7
cell line but not in MCF-7/TAM, while aspirin combined with tamoxifen can inhibit
the expression of these proteins in the resistant cell line. When knocking down
c-myc in MCF-7/TAM, cells become more sensitive to tamoxifen, cell cycle is
blocked as well, indicating that aspirin can regulate c-myc and cyclinD1 proteins
to overcome tamoxifen resistance. Our study discovered a novel role of aspirin
based on its anti-tumor effect, and put forward some kinds of possible mechanisms
of tamoxifen resistance in ER-positive breast cancer cells, providing a new
strategy for the treatment of ER-positive breast carcinoma.