• 中国科技论文统计源期刊
  • 中国科技核心期刊
  • 中国高校优秀期刊
  • 安徽省优秀科技期刊
ZHANG Cui, WU Yingling, DING Jingju, WANG Sheng, GU Yu, HE Lei, JIANG Zhengju. Role of miR-34c downregulated by EBV in promoting proliferation and migration of nasopharyngeal carcinoma cells and its mechanism[J]. Journal of Bengbu Medical University, 2024, 49(1): 13-17. DOI: 10.13898/j.cnki.issn.1000-2200.2024.01.003
Citation: ZHANG Cui, WU Yingling, DING Jingju, WANG Sheng, GU Yu, HE Lei, JIANG Zhengju. Role of miR-34c downregulated by EBV in promoting proliferation and migration of nasopharyngeal carcinoma cells and its mechanism[J]. Journal of Bengbu Medical University, 2024, 49(1): 13-17. DOI: 10.13898/j.cnki.issn.1000-2200.2024.01.003

Role of miR-34c downregulated by EBV in promoting proliferation and migration of nasopharyngeal carcinoma cells and its mechanism

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  • Received Date: April 19, 2022
  • Revised Date: February 09, 2023
  • ObjectiveTo investigate the role of miR-34c downregulated by Epstein-Barr virus (EBV) in promoting the proliferation, migration, and invasion of nasopharyngeal carcinoma cells and its mechanism.
    MethodsThe expression level of miR-34c in EBV-negative nasopharyngeal carcinoma SUNE1, CNE2, HK1 cells, and EBV-positive C666-1 cells was detected by qPCR.MiR-34c mimics were constructed to analyze the influence of miR-34c on the biological function of nasopharyngeal carcinoma cells.CCK-8, scratch healing assay, and Transwell cell invasion assay were applied to detect the proliferation, migration, and invasion ability of nasopharyngeal carcinoma cells.Western blotting was employed to determine the expression levels of migration and invasion-related proteins, and Erk1/2 signaling pathway proteins in cells.
    ResultsMiR-34c was downregulated in EBV-positive C666-1 cells (P < 0.05).CCK-8 results showed that the viability of C666-1 cells in the miR-34c group was significantly lower than that in the EBV group at 16, 24, and 48 hours (P < 0.01).The scratch assay and Transwell assay results indicated that compared with the miR-34c group, the migration and invasion ability of C666-1 cells in the EBV group were significantly enhanced (P < 0.01).Western blotting results showed that compared with the miR-34c group, the expression of migration and invasion-related proteins Vimentin, Snail, MMP-2, MMP-3, and Erk1 and Erk2 proteins of C666-1 cells in the EBV group were significantly increased (P < 0.01).
    ConclusionsMiR-34c is downregulated in EBV-positive nasopharyngeal carcinoma cells, and miR-34c downregulated by EBV can enhance the proliferation, invasion, and migration capacities of nasopharyngeal carcinoma cells and activate the Erk1/2 signaling pathway.
  • [1]
    YEW PY, MUSHIRODA T, KIYOTANI K, et al. Identification of a functional variant in SPLUNC1 associated with nasopharyngeal carcinoma susceptibility among Malaysian Chinese[J]. Mol Carcinog, 2012, 51(1): E74.
    [2]
    SU ZY, SIAK PY, LEONG CO, et al. The role of Epstein-Barr virus in nasopharyngeal carcinoma[J]. Front Microbiol, 2023, 14: 1116143. doi: 10.3389/fmicb.2023.1116143
    [3]
    PNG YT, YANG AZY, LEE MY, et al. The role of NK cells in EBV infection and EBV-associated NPC[J]. Viruses, 2021, 13(2): 300. doi: 10.3390/v13020300
    [4]
    CAI LM, LYU XM, LUO WR, et al. EBV-miR-BART7-3p promotes the EMT and metastasis of nasopharyngeal carcinoma cells by suppressing the tumor suppressor PTEN[J]. Oncogene, 2015, 34(17): 2156. doi: 10.1038/onc.2014.341
    [5]
    CUI X, SNAPPER CM. Epstein Barr virus: development of vaccines and immune cell therapy for EBV-associated diseases[J]. Front Immunol, 2021, 12: 734471. doi: 10.3389/fimmu.2021.734471
    [6]
    DAMANIA B, KENNEY SC, RAAB-TRAUB N. Epstein-Barr virus: biology and clinical disease[J]. Cell, 2022, 185(20): 3652. doi: 10.1016/j.cell.2022.08.026
    [7]
    LI R, ZHANG H, ZHENG X. MiR-34c induces apoptosis and inhibits the viability of M4e cells by targeting BCL2[J]. Oncol Lett, 2018, 15, 3357.
    [8]
    BARTOSZEWSKA S, CABAJ A, BROWSKI M, et al. miR-34c-5p modulates X-box-binding protein 1 (XBP1) expression during the adaptive phase of the unfolded protein response[J]. FASEB J, 2019, 33, 11541. doi: 10.1096/fj.201900600RR
    [9]
    XIAO SS, LI YR, PAN Q, et al. MiR-34c/SOX9 axis regulates the chemoresistance of ovarian cancer cell to cisplatin-based chemotherapy[J]. J Cell Biochem, 2019, 120, 2940. doi: 10.1002/jcb.26865
    [10]
    WANG J, LIU Y, ZHANG Y, et al. Targeting exosomes enveloped EBV-miR-BART1-5p-antagomiRs for NPC therapy through both anti-vasculogenic mimicry and anti-angiogenesis[J]. Cancer Med, 2023, 12(11): 12608. doi: 10.1002/cam4.5941
    [11]
    赵光, 朱天霸, 许儒, 等. 基于SEER数据库建立鼻咽癌预后预测模型列线图[J]. 徐州医科大学学报, 2022, 42(3): 217. https://www.cnki.com.cn/Article/CJFDTOTAL-XZYX202203012.htm
    [12]
    AHMED N, ABUSALAH M, FARZAND A, et al. Updates on Epstein-Barr virus (EBV)-associated nasopharyngeal carcinoma: emphasis on the latent gene products of EBV[J]. Medicina (Kaunas), 2022, 59(1): 2. doi: 10.3390/medicina59010002
    [13]
    XU S, ZHOU Z, PENG X, et al. EBV-LMP1 promotes radioresistance by inducing protective autophagy through BNIP3 in nasopharyngeal carcinoma[J]. Cell Death Dis, 2021, 12(4): 344. doi: 10.1038/s41419-021-03639-2
    [14]
    ZHU Q, ZHANG Q, GU M, et al. MIR106A-5p upregulation suppresses autophagy and accelerates malignant phenotype in nasopharyngeal carcinoma[J]. Autophagy, 2021, 17(7): 1667. doi: 10.1080/15548627.2020.1781368
    [15]
    GUO R, LIANG JH, ZHANG Y, et al. Methionine metabolism controls the B cell EBV epigenome and viral latency[J]. Cell Metab, 2022, 34(9): 1280. doi: 10.1016/j.cmet.2022.08.008
    [16]
    MA YX, ZHANG H, LI XH, et al. MiR-30e-5p inhibits proliferation and metastasis of nasopharyngeal carcinoma cells by targeting USP22[J]. Eur Rev Med, Pharmacol, 2018, 22, 6342.
    [17]
    KRAMER N, WALZL A, UNGER C, et al. In vitro cell migration and invasion assays[J]. Mutat Res, 2013, 752: 10. doi: 10.1016/j.mrrev.2012.08.001
    [18]
    DUFF D, LONG A. Roles for RACK1 in cancer cell migration and invasion[J]. Cell. Signal, 2017, 35, 250. doi: 10.1016/j.cellsig.2017.03.005
    [19]
    MENDEZ MG, KOJIMA S, GOLDMAN RD. Vimentin induces changes in cell shape, motility, and adhesion during the epithelial to mesenchymal transition[J]. FASEB J, 2010, 24, 1838. doi: 10.1096/fj.09-151639
    [20]
    SANG Y, CHENG C, ZENG YX, et al. Snail promotes metastasis of nasopharyngeal carcinoma partly by down-regulating TEL2[J]. Cancer Communications (London, England), 2018, 38: 58.
    [21]
    LI Y, YANG X, DU X, et al. RAB37 hypermethylation regulates metastasis and resistance to docetaxel-based induction chemotherapy in nasopharyngeal carcinoma[J]. Clin Cancer Res, 2018, 24: 6495. doi: 10.1158/1078-0432.CCR-18-0532
    [22]
    DU ZM, HU CF, SHAO Q, et al. Upregulation of caveolin-1 and CD147 expression in nasopharyngeal carcinoma enhanced tumor cell migration and correlated with poor prognosis of the patients[J]. Int J Cancer, 2019, 125: 1832.
    [23]
    KUMAR B, KOUL S, PETERSEN J, et al. p38 mitogen-activated protein kinase-driven MAPKAPK2 regulates invasion of bladder cancer by modulation of MMP-2 and MMP-9 activity[J]. Cancer Res, 2010, 70(2): 832. doi: 10.1158/0008-5472.CAN-09-2918
    [24]
    YANG J, LV X, CHEN J, et al. CCL2-CCR2 axis promotes metastasis of nasopharyngeal carcinoma by activating ERK1/2-MMP2/9 pathway[J]. Oncotarget, 2016, 7(13): 15632. doi: 10.18632/oncotarget.6695
    [25]
    YAN Q, ZENG Z, GONG Z, et al. Ebv-mir-bart10-3p facilitates epithelial-mesenchymal transition and promotes metastasis of nasopharyngeal carcinoma by targeting BTRC[J]. Oncotarget, 2015, 6(39): 41766. doi: 10.18632/oncotarget.6155
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