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低糖高乳酸环境下吉非替尼诱导HeLa细胞EGFR-TKI耐药的研究
Authors
吕育纯
李丽娜
+3 more
李明珠
李苹
林丽蓉
Publication date
1 January 2017
Publisher
Doi
Cite
Abstract
目的探讨低糖高乳酸微环境对表皮生长因子酪氨酸激酶抑制剂(EGFR-TKI)抑制HeLa细胞的影响和可能机制。方法HeLa细胞在常糖(葡萄糖10; mmol/L)和低糖高乳酸(葡萄糖3 mmol/L +乳酸2.5 mmol/L)环境下培养,并分别给予2.67; mumol/L吉非替尼干预。采用CCK-8法测定HeLa细胞生长抑制率,流式细胞术检测细胞周期,荧光定量RT-PCR检测EGFR和mTOR; mRNA水平的表达。结果与常糖组比较,低糖乳酸组24 h和72 h细胞抑制率均显著升高(P < 0.01),48; h细胞抑制率略高于常糖组。与吉非替尼阴性组比较,常糖+吉非替尼组和低糖乳酸+吉非替尼组在24、48、72 h三个时点细胞抑制率均显著上升(P <; 0.01)。与常糖组相比,低糖乳酸组48 h细胞诱导凋亡率显著上升(P <; 0.01),低糖乳酸+吉非替尼组细胞诱导凋亡率较低糖乳酸组显著降低(P < 0.01)。与常糖组比较,低糖乳酸组存活细胞的EGFR和mTOR; mRNA表达水平上调(P < 0.05)。常糖+吉非替尼组的EGFR和mTOR mRNA水平均上调(P <; 0.05)。与低糖乳酸组比较,低糖乳酸+吉非替尼组的EGFR和mTOR mRNA上调水平有显著差异(P <; 0.01)。结论高乳酸低糖环境下吉非替尼可大幅度上调存活HeLa细胞EGFR和mTOR表达水平,可能是诱导HeLa细胞抵抗EGFR-TKI的机制; 。泉州市第一医院青年科研; 泉州市科技计划项目; 国家面上项
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Last time updated on 10/06/2020