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诺必亭通过调节PARP-2/SIRT1/AMPK信号通路诱导人鼻咽癌C666-1细胞生长抑制和凋亡。

Nobiletin induces growth inhibition and apoptosis in human nasopharyngeal carcinoma C666-1 cells through regulating PARP-2/SIRT1/AMPK signaling pathway.

作者信息

Zheng Guo Dong, Hu Ping Jun, Chao Ying Xin, Zhou Ying, Yang Xiu Juan, Chen Bai Zhong, Yu Xi Yong, Cai Yi

机构信息

Key Laboratory of Molecular Target & Clinical Pharmacology State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences & the Fifth Affiliated Hospital Guangzhou Medical University Guangzhou 511436 China.

Guangdong Xinbaotang Biological Technology Co, Ltd Jiangmen China.

出版信息

Food Sci Nutr. 2019 Feb 10;7(3):1104-1112. doi: 10.1002/fsn3.953. eCollection 2019 Mar.

DOI:10.1002/fsn3.953
PMID:30918653
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6418462/
Abstract

BACKGROUND/AIM: Nobiletin, a major polymethoxyflavones (PMFs) from citri reticulatae pericarpium (CRP), can inhibit several forms of cancer proliferation. However, the effects of nobiletin on nasopharyngeal carcinoma (NPC) C666-1 cells remain largely unknown.

MATERIALS AND METHODS

Cell counting kit 8 (CCK8) assay was used to measure cell vitality. Flow cytometry was performed to measure the apoptosis rate. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot analysis were applied to determine the expression of mRNA and protein, respectively.

RESULTS

We showed that the proliferation rate of C666-1 cells was inhibited and the apoptosis rate was raised after treating with nobiletin. Moreover, nobiletin inhibited the expression of poly(ADP-ribose)polymerase-2 (PARP-2), and the tumor suppression effect of nobiletin on C666-1 is associated with PARP-2-dependent pathway.

CONCLUSION

We demonstrated for the first time that nobiletin inhibited the growth of C666-1 cells, which may be relative to its regulation on PARP-2/SIRT1/AMPK signaling pathway. Our result implied that nobiletin may serve as a strategy to treat nasopharyngeal carcinoma.

摘要

背景/目的：川陈皮素是一种从陈皮中提取的主要多甲氧基黄酮（PMFs），能够抑制多种癌症的增殖。然而，川陈皮素对鼻咽癌（NPC）C666-1细胞的影响仍不清楚。

材料与方法

采用细胞计数试剂盒8（CCK8）检测细胞活力。通过流式细胞术检测细胞凋亡率。分别应用定量实时聚合酶链反应（qRT-PCR）和蛋白质免疫印迹法检测mRNA和蛋白质的表达。

结果

我们发现川陈皮素处理后，C666-1细胞的增殖率受到抑制，凋亡率升高。此外，川陈皮素抑制了聚（ADP-核糖）聚合酶-2（PARP-2）的表达，川陈皮素对C666-1细胞的肿瘤抑制作用与PARP-2依赖的信号通路有关。

结论

我们首次证明川陈皮素抑制C666-1细胞的生长，这可能与其对PARP-2/沉默信息调节因子1/腺苷酸活化蛋白激酶（PARP-2/SIRT1/AMPK）信号通路的调控有关。我们的研究结果表明川陈皮素可能是一种治疗鼻咽癌的策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6b5/6418462/dc8db3b46cc8/FSN3-7-1104-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6b5/6418462/b3365fd7eee8/FSN3-7-1104-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6b5/6418462/c4f4a0243597/FSN3-7-1104-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6b5/6418462/362788d8a5e0/FSN3-7-1104-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6b5/6418462/8af97a5c60cb/FSN3-7-1104-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6b5/6418462/1e4e49807834/FSN3-7-1104-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6b5/6418462/dc8db3b46cc8/FSN3-7-1104-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6b5/6418462/b3365fd7eee8/FSN3-7-1104-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6b5/6418462/c4f4a0243597/FSN3-7-1104-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6b5/6418462/362788d8a5e0/FSN3-7-1104-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6b5/6418462/8af97a5c60cb/FSN3-7-1104-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6b5/6418462/1e4e49807834/FSN3-7-1104-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6b5/6418462/dc8db3b46cc8/FSN3-7-1104-g006.jpg

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