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2-脱氧-D-葡萄糖通过内分泌网膜的压力依赖途径降低HeLa细胞中的脂肪酸合成酶基因表达

Nagakatsu Harada¹, Aya Yoshikatsu², Hironori Yamamoto³

¹Department of Health and Nutrition, Faculty of Nursing and Nutrition, The University of Shimane, 151 Nishihayashigi, Izumo city, 693-8550, Shimane, Japan. n-harada@u-shimane.ac.jp.

Cell biochemistry and biophysics

|June 1, 2024

概括

2-脱氧-D-葡萄糖 (2-DG) 抑制了子宫癌细胞中的脂肪酸合成酶 (FASN) 表达. 这通过内质网膜 (ER) 应激发生,影响关键的转录因子并提供新的治疗见解.

科学领域:

生物化学生化学
分子生物学分子生物学
癌症研究癌症研究

背景情况:

脂肪酸合成酶 (FASN) 对于脂质生成至关重要,并且在癌症中经常被上调.
通过向葡萄糖代谢,2-脱氧-D-葡萄糖 (2-DG) 具有抗癌作用.
2-DG影响脂质代谢的确切机制,特别是FASN表达,需要进一步研究.

研究的目的:

为了研究2-DG对HeLa人类宫癌细胞FASN表达的影响.
阐明参与FASN的2DG介导调节的分子通路.
确定ER压力是否与2-DG抑制FASN有关.

主要方法:

用2-DG,thapsigargin或AEBSF对HeLa细胞进行治疗.
对FASN mRNA和蛋白质水平的分析.
记者测试以评估Fasn推广者的活动.
研究转录因子ATF6和SREBP1的激活.
过度表达GRP78以研究其作用.

主要成果:

2-DG显著降低了HeLa细胞中的FASNmRNA,蛋白质水平和促进剂活性.
无论是AMPK还是Sp1转录因子都没有调解2-DG对FASN的抑制作用.
细胞内膜网膜 (ER) 压力诱导剂 (thapsigargin,AEBSF) 模仿了2-DG对FASN的影响.
2-DG,thapsigargin和AEBSF可以抑制ATF6和SREBP1.1的激活.
由ER压力引起的GRP78表达的增加与抑制SREBP1和Fasn促进剂活性有关.

结论:

2-脱氧-D-葡萄糖 (2-DG) 抑制脂肪酸合成酶 (FASN) 的表达,通过一个依赖应激的内质网膜 (ER) 途径.
该机制涉及ATF6和SREBP1激活的抑制,可能通过通过GRP78.8.反抑制.
这些发现为癌症中FASN的调节提供了新的见解,并建议针对ER压力的潜在治疗策略.

关键词:

2 - 脱氧 - D - 葡萄糖2 - 脱氧 - D - 葡萄糖细胞内膜网膜应激压力脂肪酸合成酶是一种脂肪酸合成酶.这种细胞是HeLa细胞.在SREBP1中,

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