School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, China.
Reproductive Medicine Center of The 306th Hospital of PLA, Beijing, China.
Med Oncol. 2020 Apr 8;37(5):43. doi: 10.1007/s12032-020-01366-w.
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.
乳腺癌是女性最常见的癌症。虽然有几项研究表明细胞凋亡易感性蛋白 (CAS) 参与了乳腺癌的发展，但 CAS 调节乳腺癌细胞过程的潜在机制仍不清楚。在本研究中，我们探讨了 CAS 在促进乳腺癌细胞系 MCF-7 细胞增殖中的可能机制。CAS 的敲低导致细胞活力和增殖减少。此外，敲低 CAS 后细胞周期被阻滞在 G0/G1 期，cyclinD1 减少。此外，对 CAS 敲低细胞的 RNA-seq 分析表明，有 11 个基因的表达明显改变（倍数变化>2）。值得注意的是，与 shNC 细胞相比，shCAS 细胞中 cyp24a1 的表达明显增加，定量实时聚合酶链反应 (qPCR) 也证实了这一点。这些观察结果澄清了之前关于 CAS 调节的乳腺细胞细胞命运的相互矛盾的结果，并为 CAS 在乳腺癌发展中的作用提供了新的见解。
