circRNA_0001006 predicts prognosis and regulates cellular processes of triple-negative breast cancer via miR-424-5p.

IF 2.8 4区生物学 Q3 CELL BIOLOGY Cell Division Pub Date : 2023-05-16 DOI:10.1186/s13008-023-00089-4

Jiaqi Liu, Linna Kong, Wenqing Bian, Xiaona Lin, Feifei Wei, Jun Chu

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Abstract

Background: circular RNAs (circRNAs) have been considered novel biomarker candidates for human cancers, such as triple-negative breast cancer (TNBC). circ_0001006 was identified as a differentially expressed circRNA in metastatic breast cancer, but its significance and function in TNBC were unclear. The significance of circ_0001006 in TNBC was assessed and exploring its potential molecular mechanism to provide a therapeutic target for TNBC.

Results: circ_0001006 showed significant upregulation in TNBC and close association with patients' histological grade, Ki67 level, and TNM stage. Upregulated circ_0001006 could predict a worse prognosis and high risk of TNBC patients. In TNBC cells, silencing circ_0001006 suppressed cell proliferation, migration, and invasion. In mechanism, circ_0001006 could negatively regulate miR-424-5p, which mediated the inhibition of cellular processes by circ_0001006 knockdown.

Conclusions: Upregulated circ_0001006 in TNBC served as a poor prognosis predictor and tumor promoter via negatively regulating miR-424-5p.

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circRNA_0001006通过miR-424-5p预测预后并调节三阴性乳腺癌的细胞过程。

背景:环状rna (circRNAs)被认为是人类癌症的新型生物标志物候选者，如三阴性乳腺癌(TNBC)。circ_0001006在转移性乳腺癌中被鉴定为差异表达的circRNA，但其在TNBC中的意义和功能尚不清楚。评估circ_0001006在TNBC中的意义，并探索其潜在的分子机制，为TNBC提供治疗靶点。结果:circ_0001006在TNBC中表现出显著上调，且与患者的组织学分级、Ki67水平、TNM分期密切相关。circ_0001006表达上调可预测TNBC患者预后较差和风险较高。在TNBC细胞中，沉默circ_0001006可抑制细胞增殖、迁移和侵袭。在机制上，circ_0001006可以负向调节miR-424-5p, miR-424-5p通过敲低circ_0001006介导细胞过程的抑制。结论:TNBC中circ_0001006上调可通过负调控miR-424-5p作为不良预后预测因子和肿瘤启动因子。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Cell Division CELL BIOLOGY-

CiteScore

3.70

自引率

0.00%

发文量

审稿时长

>12 weeks

期刊介绍： Cell Division is an open access, peer-reviewed journal that encompasses all the molecular aspects of cell cycle control and cancer, cell growth, proliferation, survival, differentiation, signalling, gene transcription, protein synthesis, genome integrity, chromosome stability, centrosome duplication, DNA damage and DNA repair. Cell Division provides an online forum for the cell-cycle community that aims to publish articles on all exciting aspects of cell-cycle research and to bridge the gap between models of cell cycle regulation, development, and cancer biology. This forum is driven by specialized and timely research articles, reviews and commentaries focused on this fast moving field, providing an invaluable tool for cell-cycle biologists. Cell Division publishes articles in areas which includes, but not limited to: DNA replication, cell fate decisions, cell cycle & development Cell proliferation, mitosis, spindle assembly checkpoint, ubiquitin mediated degradation DNA damage & repair Apoptosis & cell death