Abstract
Amphiphysin 1 (AMPH-1) is a nerve terminals-enriched protein involved in endocytosis, and we observe that its expression is increased in breast cancer tumor in compared with normal breast. However, its function in breast cancer is unknown. Here we aim to explore the role of AMPH-1 in breast cancer cells. Knockdown of AMPH-1 in breast cancer cells promotes cell proliferation, cell cycle progression and cell migration, and attenuates cell apoptosis. Of note, knockdown of AMPH-1 promotes breast cancer progression in xenograft mouse model. These oncogenic phenotypes may be partially due to the activated EMT and ERK pathways after inhibition of AMPH-1. Oncomine analyses of multiple breast cancer patient datasets show that reduced AMPH-1 mRNA level is significantly associated with breast cancer patients having metastatic events, advanced stage, poor clinical outcomes, and Paclitaxel+FEC treatment resistance. In summary, our results identified the anti-oncogenic function of AMPH-1 in breast cancer in vitro and in vivo. Activation of AMPH-1 may be a promising approach to treat breast cancer patients.