细胞周期蛋白D1
基因沉默
细胞生长
细胞凋亡
化学
基因敲除
活力测定
癌症研究
流式细胞术
分子生物学
细胞周期
下调和上调
转移
癌症
生物
医学
基因
内科学
生物化学
作者
Linfeng Zhang,Diandian Sun,Junjie Zhang,Ying Tian
出处
期刊:Life Sciences
[Elsevier]
日期:2021-02-01
卷期号:266: 118829-118829
被引量:16
标识
DOI:10.1016/j.lfs.2020.118829
摘要
Circular RNA (circRNA) is abnormally expressed in cancers and has been linked to cancer progression, including breast cancer (BC). However, the role and mechanism of circ-UBR1 in BC progression remains to be further studied. Quantitative real-time PCR (qRT-PCR) was conducted to analyze the expression of circ-UBR1, miR-1299 and Cyclin D1 (CCND1). Cell counting kit 8 (CCK8) assay was used to measure cell viability. Cell apoptosis and cell cycle distribution were analyzed by flow cytometry. Then, the migration and invasion of cells were determined by transwell assay. Moreover, BC tumor xenograft model was built to evaluate the function of circ-UBR1 silencing on BC tumor volume and weight. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were applied to illuminate the interaction between miR-1299 and circ-UBR1 or CCND1. In addition, relative CCND1 protein expression was assessed using western blot (WB) analysis. Our results revealed that circ-UBR1 was upregulated in BC, and its silencing could inhibit BC cell proliferation, metastasis, and promote apoptosis in vitro, as well as restrain BC tumor growth in vivo. Meanwhile, we found that circ-UBR1 could sponge miR-1299, and miR-1299 inhibitor could reverse the effect of circ-UBR1 knockdown on BC cell progression. Furthermore, CCND1 was a target of miR-1299, and CCND1 overexpression could reverse the effect of miR-1299 mimic on BC cell progression. Also, the downregulation of circ-UBR1 could inhibit CCND1 expression, while this effect could be inverted by miR-1299 inhibitor. Our data indicated that circ-UBR1 might play a pro-cancer role in BC progression by regulating the miR-1299/CCND1 axis.
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