南方医科大学学报

南方医科大学学报 ›› 2013, Vol. 33 ›› Issue (04): 524-.

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2-脱氧葡萄糖可增强TRAIL诱导的口腔癌细胞凋亡的敏感性

徐锦程，黄莹莹，李阳，浦龙健，夏飞，蒋琛琛，刘浩，蒋志文   

  • 出版日期:2013-04-20 发布日期:2013-04-20

  • Online:2013-04-20 Published:2013-04-20

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摘要： 目的探讨糖基化抑制剂2-脱氧葡萄糖（2-DG）对肿瘤坏死因子相关凋亡诱导配体（TRAIL）诱导肿瘤细胞凋亡作用的影
响。方法MTT法检测不同浓度（0、0.625、1.25、2.5、5、10 mmol/L）2-DG及不同浓度2-DG与TRAIL（200 ng/ml）合用对口腔癌
细胞KB的增殖抑制作用。集落克隆法检测2-DG及TRAIL对口腔癌细胞KB的增殖抑制作用。溴化丙啶（PI）单染法检测
2-DG（5 mmol/L）对TRAIL诱导口腔癌细胞KB凋亡的影响；Western blot检测2-DG（5 mmol/L）处理口腔癌细胞KB不同时间
（0、6、16、24 h），DR5 的表达以及联合TRAIL处理后Caspase-3 的表达。结果5 mmol/L 2-DG作用于口腔癌细胞KB 24、48、
72 h细胞存活率分别为75.25%、69.06%、59.19%，但24 h细胞凋亡率仅为15.9%。5 mmol/L 2-DG与TRAIL联合作用于口腔癌
细胞KB 24 h的凋亡率为72.5%，高于TRAIL本身诱导凋亡率45.3%，并且2-DG可增强TRAIL抑制口腔癌细胞KB的集落克隆
形成的作用。2-DG上调DR5的表达并且增强Caspase-3的激活。结论2-DG能增强TRAIL诱导口腔癌细胞的凋亡，其机制可
能是上调DR5的表达及增强Caspase-3的激活。

Abstract: Objective To investigate the effect of 2-deoxy-D-glucose (2-DG) in enhancing the sensitivity of oral cancer cells to
tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis. Methods The oral cancer cell line KB was
incubated in the presence of different concentrations (0, 0.625, 1.25, 2.5, 5, and 10 mmol/L) of 2-DG with or without TRAIL (200
ng/ml). The cell viability was measured using MTT assay and cell apoptosis was detected using flow cytometry with
propidium iodide (PI) staining. KB cells treated with 5 mmol/L 2-DG with or without TRAIL for 0, 6, 16, or 24 h were examined
with Western blotting for protein expressions of death receptor 5 (DR5) and caspase-3. Results Treatment of the cells with 5
mmol/L 2-DG for 24, 48 and 72 h resulted in a cell viability of 25.25%, 69.06%, and 59.19%, respectively. Combined treatment
with 5 mmol/L 2-DG with TRAIL for 24 significantly enhanced the cell apoptotic rate (72.5%) as compared to the rate induced
by TRAIL alone (45.3%) and by 2-DG (15.9%) alone. 2-DG treatment markedly up-regulated DR5 and caspase-3 expression and
enhanced the inhibitory effect of TRAIL on cell colony formation. Conclusion 2-DG sensitizes oral cancer cells to TRAILinduced
apoptosis by up-regulating DR5 and caspase-3 expressions.