胺/氨酸丰富分离因子7 Knockdown通过调节PKM2表达抑制有氧糖解和HepG2细胞的生长,通过调节PKM2表达
Weiye Shi1, Xu Yao1, Xueyu Cao1
1College of Food Science and Biology, Hebei University of Science and Technology, Shijiazhuang 050018, China.
Current issues in molecular biology
|May 24, 2024
概括
富含氨酸/氨酸的拼接因子7 (SRSF7) 在肝细胞癌 (HCC) 中过度表达,促进瘤生长. 抑制SRSF7会减少HCC细胞的增殖,并通过降低酸盐激酶M2 (PKM2) 的下调来损害有氧糖解.
科学领域:
- 分子生物学分子生物学
- 在瘤学瘤学.
- 生物化学 生物化学
背景情况:
- 富含氨酸/氨酸的拼接因子 (SRSFs) 调节RNA拼接,并与癌症有关.
- 在肝细胞癌 (HCC) 中,SRSF7的升高调节,但其确切的作用尚不清楚.
研究的目的:
- 研究SRSF7在HCC中的表达,预后意义和分子机制.
- 确定SRSF7在HCC细胞增殖,入侵,亡和有氧糖解中的作用.
主要方法:
- 对HCC患者数据的生物信息学分析.
- 在HepG2细胞中的定量逆转录PCR (qRT-PCR) 和西斑.
- 对葡萄糖吸收,乳酸盐生产,细胞增殖,克隆性,入侵和亡的测定.
主要成果:
- 在HCC中,SRSF7显著过度表达,与预后不佳相关.
- 通过SRSF7的淘汰,抑制了HepG2细胞的增殖,克隆性和侵入性,同时增强了亡.
- 抑制SRSF7降低了葡萄糖摄取,乳酸盐生产,GLUT1和LDHA表达,增加了PKM1/PKM2的比率.
结论:
- 通过促进有氧糖解,SRSF7的过度表达驱动HCC的进展.
- 通过降低PKM2的调节和抑制糖解,SRSF7的淘汰会影响HCC的生长.
- SRSF7是HCC的潜在治疗点.
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