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揭示了基于网络药理学,acRIP-seq和实验验证的骨髓瘤 Remodelin 的药理学作用

Jia Gao¹, Peili Xu¹, Feng Wang²

¹Department of Orthopedics, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, 210011, Jiangsu, People's Republic of China.

Scientific reports

|February 12, 2024

概括

雷莫德林通过向ESR2,IGF1和MAPK1.1,抑制骨髓瘤 (OS) 细胞的增殖. 这项研究阐明了Remodelin对OS的作用机制,确定了未来治疗策略的关键治疗点.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
药理学药理学是指药理学的学科.

背景情况:

骨髓瘤 (OS) 是最常见的原发性骨癌.
雷莫德林是一种N-乙转移酶10 (NAT10) 抑制剂,在癌症中显示出治疗潜力.
雷莫德林对OS的确切作用机制尚不清楚.

研究的目的:

通过网络药理学,确定雷莫德林在骨髓瘤中的治疗点.
研究雷莫德林对OS细胞中的ac4C乙化和基因表达的影响.
通过体外实验验验证潜在的治疗点.

主要方法:

网络药理学分析以确定雷莫德林和OS的重叠目标.
acRIP-seq和RNA-seq用于分析ac4C修饰和转录组的变化.
在体外实验 (CCK-8,qRT-PCR) 验证目标基因表达和细胞增殖.

主要成果:

网络药理学确定了116个重叠的基因作为OS的潜在雷莫德林标.
acRIP-seq和RNA-seq显示了ac4C修饰和mRNA表达的显著变化.
关联分析突出了382个低乙化基因,其中ESR2,IGF1和MAPK1被确定为关键标.

结论:

雷莫德林可以抑制骨髓瘤细胞的增殖.
确定ESR2,IGF1和MAPK1是雷莫德林在骨髓瘤中的关键治疗点.
这项研究提供了关于雷莫德林的机制和OS治疗潜力的见解.

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