Panoply™ Human KDM1A Knockdown Stable Cell Line

Previous studies have shown that lysine-specific histone demethylase 1A (KDM1A) is highly expressed in various human malignancies, including triple-negative breast cancer (TNBC). However, the detailed mechanisms of its role in TNBC development remain unclear. Here, researchers found that KDM1A is highly expressed in TNBC tissues and cells, and KDM1A knockdown significantly promotes TNBC cell apoptosis and inhibits cell proliferation, invasion, migration, and stemness. USP1 can increase the stability of KDM1A through deubiquitination, and USP1 deficiency can inhibit the progression of TNBC cells by reducing KDM1A expression. Furthermore, YY1 activates KDM1A expression at the transcriptional level by directly binding to the KDM1A promoter. In addition, in a TNBC mouse model, inhibiting USP1 reduced KDM1A expression, thereby inhibiting tumor growth. Therefore, YY1 upregulation increases KDM1A expression through transcriptional activation, and USP1 stabilizes KDM1A through deubiquitination, thus promoting TNBC progression.

Here, researchers constructed KDM1A knockdown MDA-MB-231 and BT-549 cells (Figure 1A). KDM1A knockdown significantly inhibited the viability of MDA-MB-231 and BT-549 cells and reduced the number of EdU-positive cells (Figure 1B, C). Apoptosis was significantly increased in KDM1A knockdown MDA-MB-231 and BT-549 cells (Figure 1D). Furthermore, the migration and invasion abilities of KDM1A knockdown MDA-MB-231 and BT-549 cells were inhibited (Figure 1E-G). Spheroid formation assays showed that KDM1A knockdown inhibited the stemness of MDA-MB-231 and BT-549 cells (Figure 1H).

Figure 1. KDM1A knockdown repressed cell proliferation, migration, invasion, stemness, and induced cell apoptosis in TNBC cells. (Su Y, et al., 2024)