Cellular apoptosis susceptibility protein (CAS) suppresses the proliferation of breast cancer cells by upregulated cyp24a1.
Mei YeRuigang HanJianwu ShiXunda WangAllan Z ZhaoFanghong LiHao ChenPublished in: Medical oncology (Northwood, London, England) (2020)
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.
Keyphrases
- crispr cas
- genome editing
- cell cycle arrest
- induced apoptosis
- cell cycle
- cell proliferation
- single cell
- cell death
- endoplasmic reticulum stress
- rna seq
- signaling pathway
- oxidative stress
- breast cancer cells
- pi k akt
- poor prognosis
- cell therapy
- high resolution
- breast cancer risk
- long non coding rna
- polycystic ovary syndrome
- metabolic syndrome
- gene expression
- type diabetes
- dna methylation
- bone marrow
- childhood cancer
- insulin resistance
- case control