LncRNA PCIF1 通过竞争性结合 miR-326 来调控 PKM 的表达,从而促进 A549/DDP 细胞的有氧糖酵解。

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS
Wan Zhong , Chun Wang , Ye Sun
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引用次数: 0

摘要

目的利用转录组分析研究非小细胞肺癌(NSCLC)顺铂耐药的机制和治疗方法:首先,通过RNA测序、CCK-8和海马能量分析仪检测A549细胞和A549/DDP细胞的生物学特征。然后,利用 GO 和 KEGG 对差异基因进行功能富集,并构建竞争性内源性 RNA 网络图。最后,通过体外和体内实验验证了预测的生物发生途径对 A549/DDP 细胞生物学功能的影响:结果:通过富集分析和细胞生物学特性检测分析了A549和A549/DDP细胞的差异转录基因。结果表明,与 A549 细胞相比,A549/DDP 细胞对顺铂的耐药性、糖代谢信号通路和糖酵解水平均明显增加。LncRNA PCIF1是A549/DDP细胞的一个新标记,可用作调控PKM表达的分子海绵。LncRNA PCIF1靶向miR-326诱导PKM表达,促进糖酵解水平,增强A549/DDP细胞对顺铂的耐药性:LncRNA PCIF1作为A549/DDP细胞的生物标志物,较高的表达量可诱导PKM,促进细胞糖酵解,导致顺铂耐药性的发生。LncRNA PCIF1可作为治疗顺铂耐药NSCLC的潜在靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
LncRNA PCIF1 promotes aerobic glycolysis in A549/DDP cells by competitively binding miR-326 to regulate PKM expression

Objective

Utilizing transcriptome analysis to investigate the mechanisms and therapeutic approaches for cisplatin resistance in non-small cell lung cancer (NSCLC).

Methods

Firstly, the biological characters of A549 cells and A549/DDP cells were detected by RNA sequencing, CCK-8 and hippocampal energy analyzer. Then, the differential Genes were functionally enriched by GO and KEGG and the competitive endogenous RNA network map was constructed. Finally, the effects of the predicted biogenesis pathway on the biological functions of A549/DDP cells were verified by in vitro and in vivo experiments.

Result

The differentially transcribed genes of A549 and A549/DDP cells were analyzed by enrichment analysis and cell biological characteristics detection. The results showed that A549/DDP cells showed significantly increased resistance to cisplatin, glucose metabolism signaling pathway and glycolysis levels compared with A549 cells. Among glycolysis-related transcription genes, PKM had the most significant difference Fold Change is 8. LncRNA PCIF1 is a new marker of A549/DDP cells and can be used as a molecular sponge to regulate the expression of PKM. LncRNA PCIF1 targets miR-326 to induce PKM expression, promote glycolysis level, and enhance the resistance of A549/DDP cells to cisplatin.

Conclusion

LncRNA PCIF1 as biomarkers of A549/DDP cells, higher expression can induce the PKM, promote cell glycolysis, lead to the occurrence of cisplatin resistance. LncRNA PCIF1 can be considered as a potential target for treating cisplatin-resistant NSCLC.

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来源期刊
ACS Applied Bio Materials
ACS Applied Bio Materials Chemistry-Chemistry (all)
CiteScore
9.40
自引率
2.10%
发文量
464
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