Abstract
Objective: To investigate the effect of the AKT1 gene mutation hotspot E17K on the growth, proliferation, survival, and migration of breast cancer cells, based on the survival and prognosis of breast cancer patients with the AKT1 E17K mutation shown in TCGA database. Methods: The survival and incidence rates of AKT1 E17K mutation hotspots in breast cancer and other cancers were extracted from the Cancer Genome Atlas (TCGA). The recombinant eukaryotic expression plasmid AKT1 E17K-pIRES2-EGFP was constructed and transfected into breast cancer MCF-7, and MDA-MB-231 cell lines. MCF-7 and MDA-MB-231 cell lines were randomly divided into blank control groups, empty plasmid groups, and recombinant plasmid groups. The growth curve was drawn using the cell counting method. The proliferation and division of breast cancer cells were detected by CFSE fluorescent dye tracking. Apoptosis was detected by Annexin V/PI double labeling and cell vitality was detected using MTT assays, and cell migratory ability was detected by cell scratch and transwell chamber tests. Results: In breast cancer, and other cancers, the overall survival rate of patients with an AKT E17K mutation was higher than that of patients with non-point mutation, and this mutation was the most common found in breast cancer. Compared with the wild type, the growth function of mutant MCF-7 cells was inhibited (P < 0.05), as was the proliferation of MCF-7 cells expressing the AKT1 E17K mutation gene (P < 0.001). The late apoptosis rate of mutant breast cancer cells increased (P < 0.05) and the viability was lower than that of wild-type cells (P < 0.05). Mutant MDA-MB-231 cells showed increased migration ability when compared to wild-type MDA-MB-231 cells (P < 0.05). Conclusions: The expression of the AKT1 E17K mutation hotspot can inhibit the growth, proliferation, and survival ability of breast cancer cells, and promote apoptosis, while it also improves their migratory ability. The survival and prognosis of breast cancer patients with this mutation are good, which may be related to the inhibition of the PI3K/AKT/mTOR signaling pathway.