Long noncoding RNA KB-1980E6.3 promotes breast cancer progression through the PI3K/AKT signalling pathway

被引:7
|
作者
He, Lin [1 ]
Tang, Lingfeng [1 ]
Wang, Rui [2 ]
Liu, Li [1 ]
Zhu, Pengpeng [2 ]
Jiang, Kunwei [1 ]
Tu, Gang [1 ]
机构
[1] Chongqing Med Univ, Affiliated Hosp 1, Dept Endocrine & Breast Surg, 1 You Yi Rd, Chongqing 400016, Peoples R China
[2] Chongqing Med Univ, Key Lab Lab Med Diagnost, Chinese Minist Educ, Chongqing 400016, Peoples R China
基金
中国国家自然科学基金;
关键词
LncRNA KB-1980E6.3; Breast cancer; PI3K/AKT pathway; Proliferation; Invasion;
D O I
10.1016/j.prp.2022.153891
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
This research aims to investigate the effect of lncRNA KB-1980E6.3 on the biological behaviour of breast cancer cells under normoxic conditions and the underlying molecular mechanism. The expression of KB-1980E6.3 in breast cancer tissues and cells was detected by RT-qPCR. The proliferation, migration and invasion of cells were evaluated by CCK-8, colony formation, scratch and Transwell assays; KB-1980E6.3-related xenograft models were established for in vivo studies. The protein expression of PI3K, p-PI3K, AKT and p-AKT was validated by western blotting analysis. The levels of KB-1980E6.3 are significantly upregulated in breast cancer tissues and cells and are related to the poor prognosis. Functional research both in vivo and in vitro revealed that the downregulation of KB-1980E6.3 expression significantly decreased cell proliferation, invasion and migration, while ectopic KB-1980E6.3 expression obviously promoted these biological phenotypes. In terms of the mechanism, KB-1980E6.3 is involved in the activation of the PI3K/AKT signalling pathway. Knockdown of KB-1980E6.3 reduced the expression of the p-PI3K and p-AKT proteins, whereas KB-1980E6.3 overexpression showed the opposite result. The agonist 740Y-P and inhibitor LY294002 reversed the effect of KB-1980E6.3 knockdown and overexpression on the PI3K/AKT pathway in BC cells. KB-1980E6.3 promotes the proliferation, invasion and migration of breast cancer cells by activating PI3K/AKT signalling, which can be used as a potential target for breast cancer therapy.
引用
收藏
页数:10
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