PVT1 affects EMT and cell proliferation and migration via regulating p21 in triple-negative breast cancer cells cultured with mature adipogenic medium

被引:30
作者
Wang, Lingli [1 ]
Wang, Ruirui [2 ]
Ye, Zi [2 ]
Wang, Yanyan [2 ]
Li, Xiao [2 ]
Chen, Weizhen [2 ]
Zhang, Mengna [2 ]
Cai, Cheguo [2 ]
机构
[1] Guangzhou Univ Chinese Med, Math Engn Acad Chinese Med, Guangzhou 510405, Guangdong, Peoples R China
[2] Wuhan Univ, Med Res Inst, Wuhan 430071, Hubei, Peoples R China
基金
中国国家自然科学基金;
关键词
breast cancer; triple-negative breast cancer; mature adipogenic medium; PVT1; p21; LONG NONCODING RNAS; OBESITY; GROWTH; ROLES;
D O I
10.1093/abbs/gmy129
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
Excessive adiposity has long been proved to be associated with greater incidence and mortality of breast cancer in post-menopausal women. However, the effects and underlying mechanisms of human adipocytes on breast cancer cells remain largely unknown. In recent years, several reports have revealed the oncogenic role of long non-coding RNA PVT1 in breast cancer. Here, we aimed to investigate the role and underlying mechanisms of PVT1 in triple-negative breast cancer (TNBC) cells cultured with mature adipogenic medium. At first, we successfully induced adipogenic differentiation from human adipose-derived mesenchymal stem cells and collected the mature adipogenic medium to mimic excessive adiposity. Our results demonstrated that the mature adipogenic medium promoted the epithelial-mesenchymal transition, enhanced the cell viability and migration potential of TNBC cells. In addition, we proved that mature adipogenic medium affected the PVT1 expression and inhibition of the PVT1 disturbed the role of mature adipogenic medium in TNBC cells. Finally, we illustrated that repression of p21 restored the phenotype caused by PVT1 knockdown in TNBC cells treated with mature adipogenic medium. Taken together, our results demonstrated that PVT1 affected the role of mature adipogenic medium in TNBC cells via modulating p21 expression.
引用
收藏
页码:1211 / 1218
页数:8
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