Conclusions
Our results imply that EIF1AX may play a key role in the incidence and promotion of breast cancer and may, thus, serve as a valuable target for breast cancer therapy.
Methods
The expression of EIF1AX in breast cancer tissues was detected by qRT-PCR and immunohistochemistry staining. Colony formation and tumour xenograft assays were used to examine the tumorigenesis-associated function of EIF1AX in vitro and in vivo. RNA-Seq analysis was used to select the downstream target genes of EIF1AX. Flow cytometry, ChIP and luciferase assays were used to investigate the molecular mechanisms by which EIF1AX regulates p21 in breast cancer cells.
Objective
Dysregulation of the cell cycle is associated with the progression of malignant cancer, but its precise functional contribution is unknown. Materials and
Results
EIF1AX promoted breast cancer cell proliferation by promoting the G1/S cell cycle transition. A mechanistic investigation showed that EIF1AX inhibited the expression of p21, which is an essential cell cycle regulator. We identified that the transcriptional regulation of p21 by EIF1AX was p53-independent. Clinically, EIF1AX levels were significantly elevated in breast cancer tissues, and the high level of EIF1AX was associated with lower survival rates in breast cancer patients. Conclusions: Our results imply that EIF1AX may play a key role in the incidence and promotion of breast cancer and may, thus, serve as a valuable target for breast cancer therapy.