() and microRNA (miRNA) play a crucial role in breast cancer (BC), but the molecular mechanism is vague. Evidence showed that can activate (). Clinical indications of eighty BC patients were collected and the expression was detected using real-time quantitative PCR. MCF-7 and MDA-MB-231 cells were transfected with overexpression or knockdown of , , or . Cell counting kit-8, cell cloning formation, wound healing, Transwell, and flow cytometry assays were performed to investigate the malignant phenotype of BC. The dual-luciferase reporter gene analyses were applied to reveal the interaction between these target genes. Subcutaneous tumorigenic model mice were established with overexpression MDA-MB-231 cells in vivo; the tumor weight and volume, levels of and mRNA were measured. Western blot and immunohistochemistry were used to detect TRIM14 in cells and mice. levels were notably higher in BC patients and have been found to promote cell proliferation, invasion, and migration of BC cells. altered cell cycle and hindered apoptosis. knockdown or overexpression inhibited the malignant phenotype of BC. Furthermore, knockdown reversed 's promotion effects on BC. Interestingly, overexpression counteracts the inhibitory effects of overexpression and silencing on BC. Moreover, in BC tumor-bearing mice, overexpression led to increased TRIM14 expression and facilitated tumor growth. enhanced BC progression through / axis, indicating its potential as a biomarker and therapeutic target in BC.