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Dihydromyricetin promotes apoptosis, suppresses proliferation and tumor necrosis factor-α-mediated nuclear factor kappa-B activation in nasopharyngeal carcinoma CNE-2 cells

查看全文 作　　者：LI [1,2]Caihong;SHI [3]Jinlian;HUANG [4]Bo;DING [1]Hang;LIN [5]Hanguang;ZENG [2]Jincheng;ZHAO [6]Yang;LUO [7]Guoqing 高影响力作者 机构地区：[1]Institute of Biochemistry and Molecular Biology,Guangdong Medical University,Zhanjiang 524023,China;[2]Dongguan Key Laboratory of Medical Bioactive Molecular Developmental and Translational Research,Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics,Guangdong Medical University,Dongguan 523808,China;[3]Department of Otolaryngology of Shenzhen Longhua New District Central Hospital,Shenzhen 518109,China;[4]Department of Otolaryngology of The Third People's Hospital of Longgang,Shenzhen 518115,China;[5]Faculty of Forensic Medicine of Guangdong Medical University,Dongguan 523808,China;[6]Department of Otolaryngology of the Second Affiliated Hospital of Guangdong Medical University,Zhanjiang 524023,China;[7]Department of Otolaryngology of the Affiliated Hospital of Guangdong Medical University,Zhanjiang 524023,China高影响力机构 出　　处：《Journal of Traditional Chinese Medicine》索引2021年第41卷第3期,共9页高影响力期刊 基　　金：Supported by the National Natural Science Foundation of China (Regulation and Mechanism of Bone Marrow Mesenchymal Stem Cells on the Characteristics of Nasopharyngeal Carcinoma Stem Cells, No.81272434);the Medical Research Fund of Guangdong Province (Effect of Berberine on Growth of Transplanted Tumor of Nasopharyngeal Carcinoma in Mice Based on JAK/STAT3 Signaling Pathway, No.A2016431)。 摘　　要：OBJECTIVE: To investigate the efficacy of dihydromyricetin(DMY) on nasopharyngeal carcinoma(NPC) cell proliferation, apoptosis and to reveal the underlying mechanism in vitro experiments.METHODS: The CNE-2 cell line was treated with different concentrations of DMY and the effects of DMY on cell viability and proliferation were evaluated using cell counting kit-8(CCK-8) assay and plate colony formation assay. Cellular apoptosis was detected by flow cytometry following Annexin V fluorescein isothiocyanate/propidine iodide staining.Nuclei morphology was observed under a fluorescence microscope following Hoechst 333258 staining. The expression of phosphorylated inhibitor of nuclear factor kappa-B kinase subunit beta(p-IKKβ), phosphorylated inhibitor of nuclear factor kappa-B kinase subunit alpha(p-IKKα), inhibitor of nuclear factor kappa-B alpha(IκB-α), nuclear factor kappa-B(NF-κB)/p65 was examined by Western blot analysis and the nuclear translocation of NF-κB/p65 was observed using a confocal laser scanning microscopy.RESULTS: DMY inhibited the proliferative capability and colony formation of NPC CNE-2 cells. Meanwhile, DMY induced apoptosis of CNE-2 cells in a dose and time-dependent manner via upregulating B-cell lymphoma-2 associated X, but downregulating B-cell lymphoma-2 and pro-caspase-3. Importantly, we found that DMY suppressed tumor necrosis factor alpha(TNF-α)-mediated NF-κB activation via inhibiting p-IKKβ, p-IKKα and blocking NF-κB subunit p65.CONCLUSION: Our experiments demonstrated that DMY had significant antiproliferative and apoptosisinducing effects on CNE-2 cells. Additionally, DMY promoted inactivation of p-IKKβ, p-IKKα,and blocked the nuclear translocation of NF-κB subunit p65. These results suggest that DMY may be an important therapeutic approach for NPC. 关 键 词：DIHYDROMYRICETIN Nasopharyngeal carcinoma Cell proliferation Apoptosis I-kappa B kinase NF-kappa B Signal transduction
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