Genome-wide identification of alternative splicing related with transcription factors and splicing regulators in breast cancer stem cells responding to fasting-mimicking diet

IF 2.6 4区 生物学 Q2 BIOLOGY
Hongshuang Qin, Qian Zhang, Yanxiang Guo
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Abstract

Fasting-mimicking diet (FMD) can effectively inhibit the viability of breast cancer stem cells (CSCs). However, the molecular mechanisms underlying the inhibitory function of FMD on breast CSCs remain largely unknown. Elucidating the mechanisms by which FMD suppresses breast CSCs is beneficial to targeting breast CSCs. Herein, we systematically analyze alternative splicing and RNA binding protein (RBP) expression in breast CSCs during FMD. The analysis results show that a large number of regulated alternative splicing (RAS) and differentially expressed genes (DEGs) appear responding to FMD. Further studies show that there are potential regulatory relationships between transcription factors (TFs) with RAS (RAS-TFs) and their differentially expressed target genes (RAS-TF-DEGs). Moreover, differentially expressed RNA binding proteins (DERBPs) exhibit potential regulatory functions on RAS-TFs. In short, DERBPs potentially control the alternative splicing of TFs (RAS-TFs), regulating their target gene (RAS-TF-DEG) expression, which leads to the regulation of biological processes in breast CSCs during FMD. In addition, the alternative splicing and DEGs are compared between breast CSCs and differentiated cancer cells during FMD, providing new interpretations for the different responses of the two types of cells. Our studies will shed light on the understanding of the molecular mechanisms underlying breast CSC inhibition induced by FMD.
全基因组范围内鉴定乳腺癌干细胞对禁食模拟饮食反应中与转录因子和剪接调节因子相关的替代剪接
模拟空腹饮食(FMD)能有效抑制乳腺癌干细胞(CSCs)的活力。然而,FMD抑制乳腺癌干细胞的分子机制仍不为人知。阐明FMD抑制乳腺癌干细胞的机制有利于靶向治疗乳腺癌干细胞。在此,我们系统分析了FMD过程中乳腺CSCs的替代剪接和RNA结合蛋白(RBP)表达。分析结果显示,大量受调控的替代剪接(RAS)和差异表达基因(DEGs)出现了对FMD的响应。进一步的研究表明,带有 RAS 的转录因子(TFs)(RAS-TFs)与其差异表达的靶基因(RAS-TF-DEGs)之间存在潜在的调控关系。此外,差异表达的 RNA 结合蛋白(DERBPs)对 RAS-TFs 具有潜在的调控功能。简而言之,DERBPs 有可能控制 TFs(RAS-TFs)的替代剪接,调节其靶基因(RAS-TF-DEGs)的表达,从而调控 FMD 期间乳腺 CSCs 的生物学过程。此外,我们还比较了乳腺癌 CSCs 和分化癌细胞在 FMD 期间的替代剪接和 DEGs,为这两类细胞的不同反应提供了新的解释。我们的研究将有助于了解 FMD 诱导乳腺癌 CSC 抑制的分子机制。
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来源期刊
Computational Biology and Chemistry
Computational Biology and Chemistry 生物-计算机:跨学科应用
CiteScore
6.10
自引率
3.20%
发文量
142
审稿时长
24 days
期刊介绍: Computational Biology and Chemistry publishes original research papers and review articles in all areas of computational life sciences. High quality research contributions with a major computational component in the areas of nucleic acid and protein sequence research, molecular evolution, molecular genetics (functional genomics and proteomics), theory and practice of either biology-specific or chemical-biology-specific modeling, and structural biology of nucleic acids and proteins are particularly welcome. Exceptionally high quality research work in bioinformatics, systems biology, ecology, computational pharmacology, metabolism, biomedical engineering, epidemiology, and statistical genetics will also be considered. Given their inherent uncertainty, protein modeling and molecular docking studies should be thoroughly validated. In the absence of experimental results for validation, the use of molecular dynamics simulations along with detailed free energy calculations, for example, should be used as complementary techniques to support the major conclusions. Submissions of premature modeling exercises without additional biological insights will not be considered. Review articles will generally be commissioned by the editors and should not be submitted to the journal without explicit invitation. However prospective authors are welcome to send a brief (one to three pages) synopsis, which will be evaluated by the editors.
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