Xu Yajia, Jiang Chengyi
Department of Otolaryngology, Head and Neck Surgery, The First Affiliated Hospital of Bengbu Medical College, No.287 Changhuai Road, 233000, Bengbu, Anhui, China.
Genes Environ. 2024 Apr 22;46(1):10. doi: 10.1186/s41021-024-00304-w.
As a natural extraction, astaxanthin is gaining increasing attention because of its safety and anti-tumor properties. It has been reported to participate in the progression of various types of cancer such as gastric cancer and ovarian cancer. Nevertheless, the role of astaxanthin in nasopharyngeal carcinoma (NPC) has not been investigated.
The study aimed to explore the anticancer mechanism of astaxanthin in regulating NPC cell proliferation, cell cycle progression, apoptosis, migration, and invasion.
Human NPC cells (C666-1) were treated with different concentrations of astaxanthin (0, 1, 10, 20 mg/mL) followed by detection of cell viability. Then, C666-1 cell proliferation, apoptosis, cell cycle progression, invasion, and migration in response to 10 mg/mL astaxanthin, LY294002 (PI3K/AKT inhibitor) or parthenolide (PTL; NF-κB inhibitor) treatment were measured using cell counting kit-8 assay, colony forming assay, flow cytometry analyses, Transwell assay, and wound healing assay, respectively. Western blotting was performed to quantify protein levels of factors involved in PI3K/AKT and NF-κB signaling pathways, cell cycle phase markers (Cyclin D1, p21) and apoptotic markers (Bcl-2 and Bax).
C666-1 cell proliferation, invasion, and migration were significantly suppressed by astaxanthin while cell apoptosis and cell cycle arrest at G1 phase were effectively enhanced in the context of 10 mg/mL astaxanthin. Protein levels of p-AKT, p-P65 and p-IκB levels were suppressed by astaxanthin treatment. After LY294002 or PTL treatment, the suppressive impact of astaxanthin on C666-1 cell process was strengthened, accompanied by the more obvious decrease in cell activity and cell colony number, more enhanced cell apoptosis and G1 phase arrest, and further inhibited cell migration and invasion. Moreover, the inhibitory effect of astaxanthin on Cyclin D1 and Bcl-2 protein levels as well as the promoting impact of astaxanthin on p21 and Bax were also amplified in combination with LY294002 or PTL treatment.
Astaxanthin significantly suppresses NPC cell proliferation, cell cycle arrest, migration, invasion while promoting cell apoptosis by inactivating PI3K/AKT and NF-κB pathways. The study first reveals the anticancer role of astaxanthin in NPC, providing a potential candidate for NPC treatment.
虾青素作为一种天然提取物，因其安全性和抗肿瘤特性而受到越来越多的关注。据报道，它参与了胃癌和卵巢癌等多种癌症的进展。然而，虾青素在鼻咽癌（NPC）中的作用尚未得到研究。
本研究旨在探讨虾青素调节NPC细胞增殖、细胞周期进程、凋亡、迁移和侵袭的抗癌机制。
用不同浓度的虾青素（0、1、10、20mg/mL）处理人NPC细胞（C666-1），然后检测细胞活力。接着，分别使用细胞计数试剂盒-8法、集落形成试验、流式细胞术分析、Transwell试验和伤口愈合试验，检测10mg/mL虾青素、LY294002（PI3K/AKT抑制剂）或小白菊内酯（PTL；NF-κB抑制剂）处理后C666-1细胞的增殖、凋亡、细胞周期进程、侵袭和迁移情况。采用蛋白质印迹法对PI3K/AKT和NF-κB信号通路相关因子、细胞周期阶段标志物（细胞周期蛋白D1、p21）和凋亡标志物（Bcl-2和Bax）的蛋白水平进行定量分析。
虾青素显著抑制C666-1细胞的增殖、侵袭和迁移，同时在10mg/mL虾青素作用下有效增强细胞凋亡和G1期细胞周期阻滞。虾青素处理可抑制p-AKT、p-P65和p-IκB的蛋白水平。LY294002或PTL处理后，虾青素对C666-1细胞进程的抑制作用增强，伴随着细胞活性和细胞集落数量更明显的减少、细胞凋亡和G1期阻滞进一步增强，以及细胞迁移和侵袭进一步受到抑制。此外，与LY294002或PTL联合处理时，虾青素对细胞周期蛋白D1和Bcl-2蛋白水平的抑制作用以及对p21和Bax的促进作用也得到增强。
虾青素通过使PI3K/AKT和NF-κB通路失活，显著抑制NPC细胞增殖、细胞周期阻滞、迁移和侵袭，同时促进细胞凋亡。本研究首次揭示了虾青素在NPC中的抗癌作用，为NPC治疗提供了一个潜在的候选药物。
