基因敲除
细胞周期
乳腺癌
细胞生长
癌症研究
细胞凋亡
生物
癌症
细胞
活力测定
下调和上调
癌细胞
基因
遗传学
作者
Mei Ye,Ruigang Han,Jianwu Shi,Xunda Wang,Allan Z. Zhao,Li Fanghong,Hao Chen
标识
DOI:10.1007/s12032-020-01366-w
摘要
Breast cancer is the most common cancer in women. Although several studies demonstrated cellular apoptosis susceptibility protein (CAS) involved in the development of breast cancer, the underlying mechanisms of CAS regulating cell processes in the breast cancer remain elusive. In the present study, we explored the possible mechanism of CAS in contributing to the cell proliferation in the breast cancer cell line MCF-7. Knockdown of CAS led to the reduction of cell viability and proliferation. Furthermore, cell cycle was arrested in G0/G1 phase after knocking down CAS with the decrease of cyclinD1. In addition, RNA-seq analysis for the CAS knockdown cells demonstrated that total eleven genes were significantly altered (Fold changes > 2). Of note, the expression of cyp24a1 was dramatically increased in the shCAS cells compared to that of shNC cells as well as confirmed by quantitative real-time polymerase chain reaction (qPCR). These observations clarified the previous conflicting results on the cell fates of the breast cells regulated by CAS and provide new insight into the role of CAS in the development of breast cancer.
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