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YU Changyun, LIU Yong, CAO Hua. Metadherin-mediated Cell Proliferation and Paclitaxel Resistance in Nasopharyngeal Carcinoma[J]. Cancer Research on Prevention and Treatment, 2019, 46(1): 1-6. DOI: 10.3971/j.issn.1000-8578.2019.18.1000
Citation: YU Changyun, LIU Yong, CAO Hua. Metadherin-mediated Cell Proliferation and Paclitaxel Resistance in Nasopharyngeal Carcinoma[J]. Cancer Research on Prevention and Treatment, 2019, 46(1): 1-6. DOI: 10.3971/j.issn.1000-8578.2019.18.1000

Metadherin-mediated Cell Proliferation and Paclitaxel Resistance in Nasopharyngeal Carcinoma

  • Objective To explore the effect of metadherin (MTDH) on cell proliferation and paclitaxel resistance in nasopharyngeal carcinoma (NPC) patients.
    Methods The expression of MTDH was upregulated and inhibited by lentivirus-mediated MTDH cDNA and MTDH-shRNA in NPC cells, respectively. Cell proliferation, cell cycles and apoptosis were examined by CCK-8 and flow cytometry. The IC30, IC50, IC70 value of paclitaxel in NPC cells were obtained by CCK-8 assay. Then, the survival rates of MTDH overexpression cells and MTDH silence cells, stimulated with paclitaxel at IC30, IC50 and IC70, were evaluated using CCK-8 assay.
    Results MTDH overexpression enhanced the proliferation abilities of 5-8F and HNE-1 cells, while MTDH silence inhibited the proliferation abilities and greatly increased cells in G1 phase. The apoptosis was decreased by MTDH overexpression, and promoted by MTDH silence. MTDH overexpression induced paclitaxel resistance. Compared with control group, survival rate of MTDH overexpression cells in the presence of paclitaxel at IC70 and IC50 was increased. On the contrary, MTDH silence sensitized NPC cells to paclitaxel. The survival rate of MTDH silence cells in the presence of paclitaxel at IC50 and IC30 was decreased.
    Conclusion MTDH plays an important role in promoting NPC cell proliferation, and the high expression of MTDH could induce paclitaxel resistance in NPC cells.
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