Nasopharyngeal carcinoma (NPC) arises from the epithelium of the nasopharyngeal mucosa. Elderly people above the age of 65 years are more susceptible to NPC. Nasopharyngectomy is the renowned treatment procedure to NPC; however, it is too risky due to its complicated surgical procedure. Other treatment methods also reported with serious side effects such brain injury; hence, the alternative anticancer drug without any side effects was needed. Fucoxanthin is a carotenoid derived from marine algae with the numerous pharmacological functions. This study aims to examine the inhibitory potential in NPC cell proliferation via apoptosis and autophagy. The cytotoxicity of fucoxanthin on C666‐1 cells was observed by the MTT assay. The expression of autophagy‐linked proteins was assessed with immunoblotting analysis. The expression of autophagy protein LC3 was estimated using immunocytochemical analysis in C666‐1 and GFP‐LC3 transfected cells. Furthermore, the fucoxanthin‐treated C666‐1 cells were analyzed with TUNEL assay. The apoptotic level in the fucoxanthin‐treated C666‐1 cells was evaluated using acridine orange staining. Fucoxanthin significantly increased the expression of autophagy‐linked proteins which is clearly depicted in the immunoblotting analysis and immunocytochemical analysis of GFP‐tagged LC3 protein. The results of TUNEL assay of fucoxanthin‐treated C666‐1 in the presence autophagy inhibitors demonstrated the induction of autophagy by fucoxanthin. Acridine orange staining results of C666‐1 confirmed fucoxanthin decreases the expression of autophagy‐linked proteins during stressed condition thereby causes apoptosis. Our overall results authentically conclude that fucoxanthin induces autophagy and apoptosis in NPC cell line, and it can be ideal agent to treat nasopharyngeal cancer in future with further investigations.

中文翻译：

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岩藻黄质治疗通过诱导自噬机制抑制鼻咽癌细胞增殖

鼻咽癌 (NPC) 起源于鼻咽粘膜的上皮。65岁以上的老年人更易患鼻咽癌。鼻咽切除术是著名的鼻咽癌治疗方法；但由于手术过程复杂，风险太大。其他治疗方法也报告了严重的副作用，例如脑损伤；因此，需要没有任何副作用的替代抗癌药物。岩藻黄质是一种来自海藻的类胡萝卜素，具有多种药理功能。本研究旨在通过细胞凋亡和自噬检查 NPC 细胞增殖的抑制潜力。MTT法观察岩藻黄质对C666-1细胞的细胞毒性。自噬相关蛋白的表达通过免疫印迹分析进行评估。使用免疫细胞化学分析在 C666-1 和 GFP-LC3 转染细胞中评估自噬蛋白 LC3 的表达。此外，用 TUNEL 测定分析了岩藻黄质处理的 C666-1 细胞。使用吖啶橙染色评估岩藻黄质处理的 C666-1 细胞的凋亡水平。岩藻黄质显着增加了自噬连接蛋白的表达，这在 GFP 标记的 LC3 蛋白的免疫印迹分析和免疫细胞化学分析中得到了清楚的描述。在自噬抑制剂存在的情况下，岩藻黄质处理的 C666-1 的 TUNEL 测定结果表明岩藻黄质诱导自噬。C666-1 的吖啶橙染色结果证实，岩藻黄质在应激条件下会降低自噬相关蛋白的表达，从而导致细胞凋亡。