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.
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Funding
This work was sponsored by Qing Lan Project in Jiangsu Province of China. This work was also supported by the National Natural Science Foundation of China (No.81772856, 81,402,222) and Youth Fund of Shanghai Municipal Health Planning Commission (No.2017YQ054, 2017Y0117).
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The authors declare that they have no conflict of interest.
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All experimental protocols and methods were approved by the Jiangsu Agri-Animal Husbandry Vocational College. We also confirmed that all methods were performed in accordance with the relevant guidelines and regulations. Mice were bred in the Animal Core Facility by following procedures approved by the Jiangsu Agri-Animal Husbandry Vocational College of Institutional Animal Care and Use Committee.
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Yang, H., Wan, Z., Huang, C. et al. AMPH-1 is a tumor suppressor of lung cancer by inhibiting Ras-Raf-MEK-ERK signal pathway. Lasers Med Sci 34, 473–478 (2019). https://doi.org/10.1007/s10103-018-2616-4
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DOI: https://doi.org/10.1007/s10103-018-2616-4