Mechanistic target of rapamycin complex 1 (mTORC1) integrates various environmental signals to regulate cell growth and metabolism. mTORC1 activity is sensitive to changes in amino acid levels. Here, we investigated the effect of lysine on mTORC1 activity in non-small cell lung cancer (NSCLC) cells. Lysine deprivation suppressed mTORC1 activity and lysine replenishment restored the decreased mTORC1 activity in lysine-deprived cells. Supplementing growth factors, such as insulin growth factor-1 or insulin restored the decreased mTORC1 activity in serum-deprived cells. However, in serum/lysine-deprived cells, supplementing growth factors was not sufficient to restore mTORC1 activity, suggesting that growth factors could not activate mTORC1 efficiently in the absence of lysine. General control nonderepressible 2 and AMP-activated protein kinase were involved in lysine deprivation-mediated inhibition of mTORC1. Taken together, these results suggest that lysine might play role in the regulation of mTORC1 activation in NSCLC cells.

雷帕霉素 复合物1（mTORC1）的机械目标整合了各种环境信号，以调节细胞的生长和代谢。mTORC1活性对氨基酸水平的变化敏感。在这里，我们调查了赖氨酸对非小细胞肺癌（NSCLC）细胞中mTORC1活性的影响。赖氨酸剥夺抑制了mTORC1的活性，赖氨酸的补充恢复了赖氨酸剥夺的细胞中mTORC1活性的降低。补充生长因子，例如胰岛素生长因子-1或胰岛素，可以恢复血清缺乏细胞中mTORC1活性的降低。但是，在缺乏血清/赖氨酸的细胞中，补充生长因子不足以恢复mTORC1活性，这表明 在没有赖氨酸的情况下，生长因子不能有效激活mTORC1。一般控制不可抑制2和AMP激活的蛋白激酶参与赖氨酸剥夺介导的mTORC1抑制。综上所述，这些结果表明赖氨酸可能在NSCLC细胞中的mTORC1激活的调节中发挥作用。