Abstract
Amphiphysin 1 (AMPH-1) is a nerve terminal-enriched protein and it is a 128-kD protein with three identified functional domains. Some studies found that AMPH-1 was a dominant autoantigen associated with breast cancer and melanoma. However, its function in lung cancer is unknown. Here, we showed that AMPH-1 knockdown dramatically increased cell proliferation, attenuated cell apoptosis, and promoted cell cycle progression in human lung cancer cells. In vivo xenograft studies confirmed that the AMPH-1-knockdown cells were more tumorigenic than the controls. Moreover, we demonstrated that silencing AMPH-1 markedly activated Ras-Raf-MEK-ERK signal pathway. In summary, our results identified the anti-oncogenic function of AMPH-1 in lung cancer in vitro and in vivo. It is proposed that AMPH-1 may have potential as a new therapeutic target in human lung cancer treatment.