Dipalmitoylphosphatidic acid inhibits tumor growth in triple-negative breast cancer

被引:8
|
作者
Zhang, Qian-Qian [1 ]
Chen, Jian [1 ]
Zhou, Da-Lei [1 ]
Duan, You-Fa [1 ]
Qi, Cui-Ling [1 ]
Li, Jiang-Chao [1 ]
He, Xiao-Dong [1 ]
Zhang, Min [1 ]
Yang, Yong-Xia [2 ]
Wang, Lijing [1 ]
机构
[1] Guangdong Pharmaceut Univ, Vasc Biol Res Inst, Sch Basic Course, Guangzhou 510006, Guangdong, Peoples R China
[2] Guangdong Pharmaceut Univ, Sch Basic Course, Guangzhou 510006, Guangdong, Peoples R China
来源
基金
中国国家自然科学基金;
关键词
Dipalmitoylphosphatidic acid; triple-negative breast cancer; growth; angiogenesis; CELL-CYCLE ARREST; PHOSPHATIDIC-ACID; LYSOPHOSPHATIDIC ACID; PHOSPHOLIPASE-D; PANCREATIC-CANCER; EXPRESSION; PROLIFERATION; B1; OVEREXPRESSION; ACTIVATION;
D O I
10.7150/ijbs.16290
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Triple-negative breast cancer (TNBC) is a subtype of breast cancer with a poor prognosis, accounting for approximately 12-24% of breast cancer cases. Accumulating evidence has indicated that there is no effective targeted therapy available for TNBC. Dipalmitoylphosphatidic acid (DPPA) is a bioactive phospholipid. However, the function of DPPA in the growth of TNBC has not yet been studied. In this study, we employed TNBC cells and a subcutaneous tumor model to elucidate the possible effect of DPPA on tumor growth in TNBC. We showed that DPPA significantly inhibited tumor growth in the mouse subcutaneous tumor model and suppressed cell proliferation and angiogenesis in TNBC tumor tissues. This inhibition was mediated partly by suppressing the expression of cyclin B1 (CCNB1), which directly promoted the accumulation of cells in the G2 phase and arrested cell cycle progression in human TNBC. In addition, the inhibition of tumor growth by DPPA may also be mediated by the suppression of tumor angiogenesis in TNBC. This work provides initial evidence that DPPA might be vital as an anti-tumor drug to treat TNBC.
引用
收藏
页码:471 / 479
页数:9
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