LOXL1-AS1通过miR-1224-5p/ITPRIPL2/AKT轴促进肝细胞癌细胞增殖
Tangen Chen1, Shuyun Zeng2, Quanyuan Liu1
1Department of Hepatobiliary Surgery, Zhangzhou Municipal Hospital of Fujian Province, Zhangzhou 363000, Fujian Province, China. mahuang357069@163.com.
Cellular and molecular biology (Noisy-le-Grand, France)
|September 16, 2023
概括
长非编码RNA (lncRNA) LOXL1-AS1通过激活AKT通路和调节miR-1224-5p/ITPRIPL2.2,促进肝细胞癌 (HCC). 这项研究揭示了HCC进展中的新型lncRNA调节机制.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 遗传学 遗传学 是一个
背景情况:
- 长非编码RNAs (lncRNAs) 与各种癌症有关,但它们在肝细胞癌 (HCC) 中的特定作用尚未完全理解.
- 了解HCC中lncRNAs的调节机制对于开发向疗法至关重要.
研究的目的:
- 研究LOXL1-AS1在肝细胞癌 (HCC) 进展中的作用.
- 阐明LOXL1-AS1影响HCC细胞增殖,亡和AKT通路的分子机制.
- 在LOXL1-AS1/miR-1224-5p/ITPRIPL2轴内识别潜在的治疗点.
主要方法:
- 定量实时PCR (qRT-PCR) 来评估LOXL1-AS1和miR-1224-5p的表达.
- 细胞增殖试验 (例如,MTT,EDU) 和亡试验 (例如,流细胞计).
- 西部涂抹以评估AKT通路激活和ITPRIPL2蛋白水平.
- 路西法酶记者测定证实了LOXL1-AS1和miR-1224-5p之间的相互作用,以及miR-1224-5p与ITPRIPL2.2之间的相互作用.
主要成果:
- 在HCC细胞系中,LOXL1-AS1显著过度表达.
- 击败LOXL1-AS1抑制了HCC细胞增殖和诱导的亡.
- LOXL1-AS1激活了AKT通路,并充当了miR-1224-5p的海绵.
- ITPRIPL2被确定为miR-1224-5p的基因,其缺乏抑制了HCC细胞增殖.
- 恢复miR-1224-5p部分扭转了LOXL1-AS1耗尽的影响,ITPRIPL2沉默取消了这一效应.
结论:
- 通过激活AKT通路,LOXL1-AS1促进HCC细胞的增殖,并抑制细胞亡.
- 洛克斯L1-AS1通过海绵化miR-1224-5p,然后通过上调ITPRIPL2.2来发挥其致癌功能.
- LOXL1-AS1/miR-1224-5p/ITPRIPL2轴代表了肝细胞癌的潜在治疗标.
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