对非编码 RNA 在乳腺癌进展过程中对 TGF-β1 刺激的活化转录因子 3 的作用进行全面的生物信息学分析

IF 2.6 4区 生物学 Q2 BIOLOGY
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引用次数: 0

摘要

转化生长因子β1(TGF-β1)是正常乳腺上皮细胞的一种强效生长抑制因子。当乳腺组织失去这种因子的抗增殖活性时,侵袭和骨转移就会增加。人类乳腺癌(hBC)细胞暴露于 TGF-β1 时会表达更多的活化转录因子 3(ATF3),这种转录因子对 BC 的发展和骨转移至关重要。非编码 RNA(ncRNA),包括环状 RNA(circRNA)和微 RNA(miRNA),已成为控制多种细胞过程的关键调控因子。在 hBC 细胞中,TGF-β1 刺激了 hsa-miR-4653-5p 的表达,而 hsa-miR-4653-5p 可能是 ATF3 的靶标。生物信息学分析预测,hsa-miR-4653-5p靶向多个关键信号转导元件和转录因子,包括NFKB1、STAT1、STAT3、NOTCH1、JUN、TCF3、p300、NRF2、SUMO2和NANOG,这表明hsa-miR-4653-5p在生理和病理条件下发挥着多样化的作用。尽管hsa-miR-4653-5p在hBC细胞中含量很高,但ATF3水平仍然升高,这表明其他ncRNA可以抑制hsa-miR-4653-5p的活性。硅学分析发现了几个与hsa-miR-4653-5p有结合位点的circRNA,这表明circRNA对hsa-miR-4653-5p具有海绵活性。研究结果表明,TGF-β1可调控circRNAs和hsa-miR-4653-5p,进而影响ATF3的表达,从而影响BC的进展和骨转移。因此,关注TGF-β1/circRNAs/hsa-miR-4653-5p/ATF3网络可为诊断和治疗BC提供新方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A comprehensive bioinformatic analysis of the role of TGF-β1-stimulated activating transcription factor 3 by non-coding RNAs during breast cancer progression

A potent growth inhibitor for normal mammary epithelial cells is transforming growth factor beta 1 (TGF-β1). When breast tissues lose the anti-proliferative activity of this factor, invasion and bone metastases increase. Human breast cancer (hBC) cells express more activating transcription factor 3 (ATF3) when exposed to TGF-β1, and this transcription factor is essential for BC development and bone metastases. Non-coding RNAs (ncRNAs), including circular RNAs (circRNAs) and microRNAs (miRNAs), have emerged as key regulators controlling several cellular processes. In hBC cells, TGF-β1 stimulated the expression of hsa-miR-4653–5p that putatively targets ATF3. Bioinformatics analysis predicted that hsa-miR-4653–5p targets several key signaling components and transcription factors, including NFKB1, STAT1, STAT3, NOTCH1, JUN, TCF3, p300, NRF2, SUMO2, and NANOG, suggesting the diversified role of hsa-miR-4653–5p under physiological and pathological conditions. Despite the high abundance of hsa-miR-4653–5p in hBC cells, the ATF3 level remained elevated, indicating other ncRNAs could inhibit hsa-miR-4653–5p’s activity. In silico analysis identified several circRNAs having the binding sites for hsa-miR-4653–5p, indicating the sponging activity of circRNAs towards hsa-miR-4653–5p. The study's findings suggest that TGF-β1 regulates circRNAs and hsa-miR-4653–5p, which in turn affects ATF3 expression, thus influencing BC progression and bone metastasis. Therefore, focusing on the TGF-β1/circRNAs/hsa-miR-4653–5p/ATF3 network could lead to new ways of diagnosing and treating BC.

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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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