Dihydromyricetin promotes apoptosis, suppresses proliferation and tumor necrosis factor-α-mediated nuclear factor kappa-B activation in nasopharyngeal carcinoma CNE-2 cellsEnglish Full Text
LI Caihong;SHI Jinlian;HUANG Bo;DING Hang;LIN Hanguang;ZENG Jincheng;ZHAO Yang;LUO Guoqing;Institute of Biochemistry and Molecular Biology, Guangdong Medical University;Dongguan Key Laboratory of Medical Bioactive Molecular Developmental and Translational Research, Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics,Guangdong Medical University;Department of Otolaryngology of Shenzhen Longhua New District Central Hospital;Department of Otolaryngology of The Third People’s Hospital of Longgang;Faculty of Forensic Medicine of Guangdong Medical University;Dongguan Key Laboratory of Medical Bioactive Molecular Developmental and Translational Research,Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, Guangdong Medical University;Department of Otolaryngology of the Second Affiliated Hospital of Guangdong Medical University;Department of Otolaryngology of the Affiliated Hospital of Guangdong Medical University;
Abstract: 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.
Keywords：
Dihydromyricetin; Nasopharyngeal carcinoma; Cell proliferation; Apoptosis; I-kappa B kinase; NF-kappa B; Signal transduction;
- DOI：
10.19852/j.cnki.jtcm.2021.03.004
- Series：
(E) Medicine ＆ Public Health
- Subject：
Traditional Chinese Medicinal Herbs
- Classification Code：
R285
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