EMP1 regulates cell proliferation, migration and invasion in triple negative breast cancer through PI3K-AKT signaling.

INTRODUCTION: Triple negative breast cancer (TNBC) is characterized by high malignancy and poor prognosis due to the lack of a clear therapeutic target. The search for therapeutic targets for TNBC has always been a focus of research in the field of human oncology. Existing studies have shown that Epithelial membrane protein 1 (EMP1) is abnormally expressed in a variety of cancers and is closely related to the occurrence and development of tumors. However, the potential role and molecular mechanism of EMP1 in TNBC are still unclear. METHODS: In our study, we detected the expression levels of EMP1 in TNBC and analyzed the biological behavior of the TNBC cell line MDA-MB-231 after EMP1 expression changes. RESULTS: The results showed that the expression level of EMP1 in TNBC was lower than that in normal tissues, and its expression level was related to T stage, lymph node metastasis, clinical stage and overall survival. In addition, overexpression of EMP1 inhibited the proliferation, migration and invasion of MDA-MB-231, while the proliferation, migration and invasion of MDA-MB-231 cells were enhanced after the expression of EMP1 decreased. EMP1 functions through the PI3K-AKT pathway. DISCUSSION: In summary, our findings suggest that EMP1 plays a biological role as a tumor suppressor in TNBC.