Li Weimin, Wang Zhonglue, Chen Yina, Wang Kaijing, Lu Ting, Ying Fei, Fan Mengdi, Li Zhiyin, Wu Jiansheng
Department of Gastroenterology, The Affiliated Hospital of Hangzhou Normal University, Hangzhou, Zhejiang 310000, P.R. China.
Department of Gastroenterology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China.
Oncol Lett. 2017 Apr;13(4):2737-2744. doi: 10.3892/ol.2017.5785. Epub 2017 Feb 28.
Melatonin, which is synthesized by the pineal gland and released into the blood, exhibits antitumor properties. However, the mechanisms underlying these effects, particularly in stomach cancer, remain unknown. In the present study, the effect of melatonin on the nuclear factor (NF)-κB signaling pathway and the mitogen-activated protein kinase signaling pathway, involving p38 and c-Jun-N-terminal kinase (JNK), were investigated in SGC7901 gastric cancer cells. In addition, the effect of melatonin on the survival, migration and apoptosis of these cells was investigated in order to evaluate the use of melatonin for the treatment of gastric cancer. The results of the present study revealed that melatonin decreased the viability and migration of SGC7901 cells. Furthermore, melatonin induced apoptosis. Melatonin was identified to elevate the expression levels of phosphorylated (p)-p38 and p-JNK protein, and decrease the expression level of nucleic p-p65. These results suggest that the protein levels of p65, p38 and JNK are associated with the survival of SGC7901 cells following treatment with melatonin. The optimal concentration of melatonin was demonstrated to be 2 mM, which significantly induced apoptosis following a 24 h treatment period. These findings suggest that conflicting growth signals in cells may inhibit the efficacy of melatonin in the treatment of gastric cancer. Therefore, adjunct therapy would be required to improve the efficacy of melatonin in the treatment of cancer.
褪黑素由松果体合成并释放到血液中，具有抗肿瘤特性。然而，这些作用的潜在机制，尤其是在胃癌中的机制，仍然未知。在本研究中，在SGC7901胃癌细胞中研究了褪黑素对核因子（NF）-κB信号通路以及涉及p38和c-Jun氨基末端激酶（JNK）的丝裂原活化蛋白激酶信号通路的影响。此外，研究了褪黑素对这些细胞存活、迁移和凋亡的影响，以评估褪黑素在治疗胃癌中的应用。本研究结果显示，褪黑素降低了SGC7901细胞的活力和迁移能力。此外，褪黑素诱导了细胞凋亡。已确定褪黑素可提高磷酸化（p）-p38和p-JNK蛋白的表达水平，并降低细胞核p-p65的表达水平。这些结果表明，p65、p38和JNK的蛋白水平与褪黑素处理后SGC7901细胞的存活有关。褪黑素的最佳浓度被证明为2 mM，在24小时的处理期后可显著诱导细胞凋亡。这些发现表明，细胞中相互冲突的生长信号可能会抑制褪黑素在治疗胃癌中的疗效。因此，需要辅助治疗来提高褪黑素治疗癌症的疗效。
