MYSM1 induces apoptosis and sensitizes TNBC cells to cisplatin via RSK3-phospho-BAD pathway.
Xiaolin GuanXin MengKeyu ZhuJinyan KaiYixuan LiuQian MaYing TongHui ZhengSuhong XieXiaolu MaYanchun WangRen-Quan LuLin GuoPublished in: Cell death discovery (2022)
Breast cancer is one of the leading causes of mortality among women. Triple-negative breast cancer (TNBC) is responsible for a large percentage of all breast cancer deaths in women. This study demonstrated the function of Myb-like, SWIRM, and MPN domains 1 (MYSM1), an H2A deubiquitinase (DUB), in TNBC. MYSM1 expression was drastically decreased in breast cancer, especially in TNBC, suggesting a potential anticancer effect. Overexpressing and suppressing MYSM1 expression in TNBC cell lines led to significant biological changes in cell proliferation. Furthermore, MYSM1 overexpression increased cisplatin-induced apoptosis, which might be attributed to RSK3 inactivation and the subsequently decreased phosphorylation of Bcl-2 antagonist of cell death (BAD) (Ser 112). The findings suggest that MYSM1 is a potential target for regulating cell apoptosis and suppressing resistance to cisplatin in TNBC.
Keyphrases
- induced apoptosis
- signaling pathway
- cell proliferation
- endoplasmic reticulum stress
- oxidative stress
- cell death
- poor prognosis
- breast cancer risk
- polycystic ovary syndrome
- pi k akt
- cell cycle arrest
- cell cycle
- cardiovascular disease
- pregnancy outcomes
- binding protein
- coronary artery disease
- human health
- pregnant women
- type diabetes
- risk factors