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

作     者：LI Caihong SHI Jinlian HUANG Bo DING Hang LIN Hanguang ZENG Jincheng ZHAO Yang LUO Guoqing LI Caihong;SHI Jinlian;HUANG Bo;DING Hang;LIN Hanguang;ZENG Jincheng;ZHAO Yang;LUO Guoqing

作者机构：Institute of Biochemistry and Molecular BiologyGuangdong Medical UniversityZhanjiang 524023China Dongguan Key Laboratory of Medical Bioactive Molecular Developmental and Translational ResearchGuangdong Provincial Key Laboratory of Medical Molecular DiagnosticsGuangdong Medical UniversityDongguan 523808China Department of Otolaryngology of Shenzhen Longhua New District Central HospitalShenzhen 518109China Department of Otolaryngology of The Third People's Hospital of LonggangShenzhen 518115China Faculty of Forensic Medicine of Guangdong Medical UniversityDongguan 523808China Department of Otolaryngology of the Second Affiliated Hospital of Guangdong Medical UniversityZhanjiang 524023China Department of Otolaryngology of the Affiliated Hospital of Guangdong Medical UniversityZhanjiang 524023China 

出 版 物：《Journal of Traditional Chinese Medicine》 (中医杂志（英文版）)

年 卷 期：2021年第41卷第3期

页      面：367-375页

核心收录：

学科分类：1008[医学-中药学(可授医学、理学学位)] 1007[医学-药学(可授医学、理学学位)] 1006[医学-中西医结合] 1005[医学-中医学] 1002[医学-临床医学] 100602[医学-中西医结合临床] 10[医学] 

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) 

主　　题：Dihydromyricetin Nasopharyngeal carcinoma Cell proliferation Apoptosis I-kappa B kinase NF-kappa B Signal transduction 

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 ***: 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 *** 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 ***: 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 ***: 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.