Nasopharyngeal cancer is a malignancy developing from the nasopharynx epithelium due to smoking and nitrosamine‐containing foods. Nasopharyngeal cancer is highly endemic to Southeast Asia. Eugenol and piperine have shown many anticancer activities on numerous cancer types, like colon, lung, liver, and breast cancer. In this study, we amalgamated eugenol and piperine loaded with a polyhydroxy butyrate/polyethylene glycol nanocomposite (Eu‐Pi/PHB‐PEG‐NC) for better anticancer results against nasopharyngeal cancer (C666‐1) cells. In the current study, nasopharyngeal cancer cell lines C666‐1 were utilized to appraise the cytotoxic potential of Eug‐Pip‐PEG‐NC on cell propagation, programmed cell death, and relocation. Eu‐Pi/PHB‐PEG‐NC inhibits cellular proliferation on C666‐1 cells in a dose‐dependent manner, and when compared with 20 µg/ml, 15 µg/ml of loaded mixture evidently restrained the passage aptitude of C666‐1 cells, this was attended with a downregulated expression of mitochondrial membrane potential. Treatment with 15 µg/ml Eu‐Pi/PHB‐PEG‐NC suggestively amplified cell apoptosis in the C666‐1 cells. Furthermore, its cleaved caspase‐3, 8, and 9 and Bax gene expression was augmented and Bcl‐2 gene expression was diminished after Eu‐Pi/PHB‐PEG‐NC treatment. Additionally, our data established that the collective effect of Eu‐Pi/PHB‐PEG‐NC loaded micelles inhibited the expansion of C666‐1 cells augmented apoptosis connected with the intrusion of PI3K/Akt/mTOR signaling pathway.

中文翻译：

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丁香酚-胡椒碱负载多羟基丁酸酯/聚乙二醇纳米复合材料通过抑制PI3K / AKT / mTOR信号传导途径诱导鼻咽癌（C666-1）细胞凋亡和细胞死亡

鼻咽癌是由于吸烟和含亚硝胺的食物而从鼻咽上皮发展而来的恶性肿瘤。鼻咽癌在东南亚高度流行。丁香酚和胡椒碱已显示出对多种癌症类型的多种抗癌活性，例如结肠癌，肺癌，肝癌和乳腺癌。在这项研究中，我们将丁香酚和胡椒碱合并了多羟基丁酸酯/聚乙二醇纳米复合材料（Eu-Pi / PHB-PEG-NC），以更好地抗鼻咽癌（C666-1）细胞的抗癌效果。在本研究中，鼻咽癌细胞系C666-1被用于评估Eug-Pip-PEG-NC对细胞增殖，程序性细胞死亡和重定位的细胞毒性潜力。Eu‐Pi / PHB‐PEG‐NC以剂量依赖的方式抑制C666-1细胞的细胞增殖，与20 µg / ml相比，15 µg / ml的上样混合物明显抑制了C666-1细胞的传代能力，这伴随着线粒体膜电位表达的下调。用15 µg / ml Eu-Pi / PHB-PEG-NC处理提示C666-1细胞中的细胞凋亡。此外，在Eu-Pi / PHB-PEG-NC处理后，其裂解的caspase-3、8和9和Bax基因表达增加，Bcl-2基因表达减少。此外，我们的数据证实，负载Eu-Pi / PHB-PEG-NC的胶束的集体效应抑制了C666-1细胞的扩增，从而增加了细胞凋亡，并伴随着PI3K / Akt / mTOR信号通路的入侵。用15 µg / ml Eu-Pi / PHB-PEG-NC处理提示C666-1细胞中的细胞凋亡。此外，在Eu-Pi / PHB-PEG-NC处理后，其裂解的caspase-3、8和9和Bax基因表达增加，Bcl-2基因表达减少。此外，我们的数据证实，负载Eu-Pi / PHB-PEG-NC的胶束的集体效应抑制了C666-1细胞的扩增，从而增加了细胞凋亡，并伴随着PI3K / Akt / mTOR信号通路的入侵。用15 µg / ml Eu-Pi / PHB-PEG-NC处理提示C666-1细胞中的细胞凋亡。此外，在Eu-Pi / PHB-PEG-NC处理后，其裂解的caspase-3、8和9和Bax基因表达增加，Bcl-2基因表达减少。此外，我们的数据证实，负载Eu-Pi / PHB-PEG-NC的胶束的集体效应抑制了C666-1细胞的扩增，从而增加了细胞凋亡，并伴随着PI3K / Akt / mTOR信号通路的入侵。