J Cancer 2018; 9(12):2175-2182. doi:10.7150/jca.25428 This issue
1. Department of Clinical Laboratory, Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Nanjing Maternity and Child Health Care Hospital, Nanjing 210004, China.
2. Reproductive & Developmental Biology Laboratory, National Institute of Environmental Health Sciences (NIEHS), Research Triangle Prk, NC 27709, USA.
3. East China Normal University, 500 Dongchuan Road, Shanghai 200241, China.
4. Dongtai People,s Hospital, The Affiliated Hospital of Nantong University, 2 Kangfu Road, Yancheng 224000, China.
5. Shanghai Municipal Hospital of Tranditional Chinese Medicine, 274 Zhijingzhong Road, Shanghai 200071, China.
*These authors contributed equally to this work.
‡Authors with equal contribution
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.
Keywords: Amphiphysin 1, AMPH-1, breast cancer, apoptosis, migration, p-Erk1/2