Beijing Advanced Innovation Center for Food Nutrition and Human Health, Beijing Engineering and Technology Research Center of Food Additives, Beijing Technology and Business University, Beijing 100048, China.
State Key Laboratory of Infection Disease Prevention and Control, National Institute for Communicable Disease Control and Prevention, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Disease, Chinese Center for Disease Control and Prevention, Beijing 102206, China.
Cells. 2019 Jun 14;8(6):588. doi: 10.3390/cells8060588.
Phycocyanin is a type of marine functional food additive, exerting a health care efficacy with no side effects. It has been shown that phycocyanin possesses anticancer function in non-small cell lung cancer (NSCLC) cells, but the underlying regulatory mechanism still remains unclear. Further investigation on the antineoplastic mechanism of phycocyanin would provide useful information on NSCLC treatment. In this study, we explored the in vitro function and mechanism of phycocyanin in three typical NSCLC cell lines, H1975, H1650, and LTEP-a2, for the first time. Phenotypic experiments showed that phycocyanin significantly induced the apoptosis as well as suppressed the growth of NSCLC cells. Transcriptome analysis suggested that toll/interleukin 1 receptor domain-containing adaptor protein (TIRAP) was significantly down-regulated by phycocyanin. Strikingly, similar to phycocyanin-treated assays, siRNA knockdown of TIRAP expression also resulted in the anti-proliferative phenomenon in NSCLC cells. In addition, the activity of NF-κB signaling was also suppressed after silencing TIRAP expression, revealing that phycocyanin exerted anti-proliferative function through down-regulating TIRAP/NF-κB activity in NSCLC cells. Collectively, this study has laid a theoretical basis on the treatment of NSCLC and the potential utilization of marine functional products.
藻蓝蛋白是一种海洋功能性食品添加剂，具有保健功效且无副作用。研究表明，藻蓝蛋白对非小细胞肺癌（NSCLC）细胞具有抗癌作用，但具体的调控机制尚不清楚。进一步研究藻蓝蛋白的抗肿瘤机制，将为 NSCLC 的治疗提供有用的信息。本研究首次探讨了藻蓝蛋白在三种典型的 NSCLC 细胞系 H1975、H1650 和 LTEP-a2 中的体外功能和作用机制。表型实验表明，藻蓝蛋白能显著诱导 NSCLC 细胞凋亡并抑制其生长。转录组分析表明，藻蓝蛋白显著下调 Toll/IL-1 受体结构域包含衔接蛋白（TIRAP）的表达。值得注意的是，与藻蓝蛋白处理实验类似，TIRAP 表达的 siRNA 敲低也导致 NSCLC 细胞的抗增殖现象。此外，沉默 TIRAP 表达后 NF-κB 信号通路的活性也受到抑制，表明藻蓝蛋白通过下调 TIRAP/NF-κB 活性在 NSCLC 细胞中发挥抗增殖作用。综上所述，本研究为 NSCLC 的治疗和海洋功能产品的潜在应用奠定了理论基础。
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