蛋白激酶B
PI3K/AKT/mTOR通路
基因沉默
自噬
癌症研究
细胞生长
原癌基因酪氨酸蛋白激酶Src
细胞生物学
化学
细胞凋亡
基因敲除
癌细胞
信号转导
生物
癌症
生物化学
基因
遗传学
标识
DOI:10.1016/j.repbio.2021.100538
摘要
Breast cancer (BC) is the major reason of cancer deaths in females. However, the underlying mechanism remains to be elucidated. F-box and leucine-rich repeat protein 16 (FBXL16) is known to be an important protein in regulating cancer growth. Nonetheless, little is known about FBXL16 in BC. Herein, FBXL16 protein expression was found to be elevated in the tumor tissues of BC patients and BC cell lines (MDA-MB-231, MCF-7, MDA-MB-361, and T47D). FBXL16 silencing inhibited cell growth and increased cell apoptosis as well as cell autophagy in MDA-MB-231 and MCF-7 cells, indicating that FBXL16 could aggravate malignant behaviors in BC. Moreover, FBXL16 deficiency was demonstrated to reduce the level of steroid receptor coactivator 3 (SRC-3) in MDA-MB-231 and MCF-7 cells. FBXL16 silencing also suppressed the level of p-AKT and p-mTOR. Whereas SCR-3 overexpression reversed FBXL16 knockdown-mediated p-AKT and p-mTOR reduction. Rescue assays uncovered that SRC-3 overexpression offset FBXL16 silencing-mediated decrease in cell proliferation and increase in cell apoptosis and autography in MDA-MB-231 and MCF-7 cells. In conclusion, our study found that FBXL16 modulates cell proliferation and autophagy in BC cells via activating the SRC-3-AKT signaling pathway, which shed a light on potential novel biomarkers for the treatment of BC.
科研通智能强力驱动
Strongly Powered by AbleSci AI