Circ_RPPH1 通过 miR-1296-5p/TRIM14 轴促进乳腺癌的进展。

IF 4.4 4区 医学 Q2 ONCOLOGY Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-05-30 DOI:10.1080/15384047.2024.2360768
Jing Jiang, Shenghong Shi, Wei Zhang, Chao Li, Long Sun, Qidong Ge, Xujun Li
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引用次数: 0

摘要

环状 RNA 核糖核酸酶 P RNA 成分 H1(circ_RPPH1)和 microRNA(miRNA)miR-1296-5p 在乳腺癌(BC)中起着至关重要的作用,但其分子机制尚不清楚。有证据表明,miR-1296-5p 能激活含三方基序 14(TRIM14)。研究人员收集了 80 例 BC 患者的临床指征,并使用实时定量 PCR 检测了 circ_RPPH1 的表达。用过表达或敲除 circ_RPPH1、miR-1296-5p 或 TRIM14 的方法转染 MCF-7 和 MDA-MB-231 细胞。进行了细胞计数试剂盒-8、细胞克隆形成、伤口愈合、Transwell 和流式细胞术检测,以研究 BC 的恶性表型。应用双荧光素酶报告基因分析揭示了这些靶基因之间的相互作用。用circ_RPPH1过表达的MDA-MB-231细胞建立皮下肿瘤模型小鼠,测量肿瘤的重量和体积、miR-1296-5和TRIM14 mRNA的水平。采用 Western 印迹和免疫组织化学方法检测细胞和小鼠中的 TRIM14。BC患者的Circ_RPPH1水平明显较高,研究发现它能促进BC细胞的增殖、侵袭和迁移。Circ_RPPH1会改变细胞周期并阻碍细胞凋亡。Circ_RPPH1敲除或miR-1296-5p过表达可抑制BC的恶性表型。此外,miR-1296-5p 的敲除逆转了 circ_RPPH1 对 BC 的促进作用。有趣的是,TRIM14 的过表达抵消了 miR-1296-5p 过表达和 circ_RPPH1 沉默对 BC 的抑制作用。此外,在BC肿瘤小鼠中,circ_RPPH1过表达会导致TRIM14表达增加,并促进肿瘤生长。circ_RPPH1通过miR-1296-5p/TRIM14轴促进了BC的进展,表明它有可能成为BC的生物标记物和治疗靶点。
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Circ_RPPH1 facilitates progression of breast cancer via miR-1296-5p/TRIM14 axis.

Circular RNA Ribonuclease P RNA Component H1 (circ_RPPH1) and microRNA (miRNA) miR-1296-5p play a crucial role in breast cancer (BC), but the molecular mechanism is vague. Evidence showed that miR-1296-5p can activate tripartite motif-containing 14 (TRIM14). Clinical indications of eighty BC patients were collected and the circ_RPPH1 expression was detected using real-time quantitative PCR. MCF-7 and MDA-MB-231 cells were transfected with overexpression or knockdown of circ_RPPH1, miR-1296-5p, or TRIM14. Cell counting kit-8, cell cloning formation, wound healing, Transwell, and flow cytometry assays were performed to investigate the malignant phenotype of BC. The dual-luciferase reporter gene analyses were applied to reveal the interaction between these target genes. Subcutaneous tumorigenic model mice were established with circ_RPPH1 overexpression MDA-MB-231 cells in vivo; the tumor weight and volume, levels of miR-1296-5 and TRIM14 mRNA were measured. Western blot and immunohistochemistry were used to detect TRIM14 in cells and mice. Circ_RPPH1 levels were notably higher in BC patients and have been found to promote cell proliferation, invasion, and migration of BC cells. Circ_RPPH1 altered cell cycle and hindered apoptosis. Circ_RPPH1 knockdown or miR-1296-5p overexpression inhibited the malignant phenotype of BC. Furthermore, miR-1296-5p knockdown reversed circ_RPPH1's promotion effects on BC. Interestingly, TRIM14 overexpression counteracts the inhibitory effects of miR-1296-5p overexpression and circ_RPPH1 silencing on BC. Moreover, in BC tumor-bearing mice, circ_RPPH1 overexpression led to increased TRIM14 expression and facilitated tumor growth. Circ_RPPH1 enhanced BC progression through miR-1296-5p/TRIM14 axis, indicating its potential as a biomarker and therapeutic target in BC.

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来源期刊
Cancer Biology & Therapy
Cancer Biology & Therapy 医学-肿瘤学
CiteScore
7.00
自引率
0.00%
发文量
60
审稿时长
2.3 months
期刊介绍: Cancer, the second leading cause of death, is a heterogenous group of over 100 diseases. Cancer is characterized by disordered and deregulated cellular and stromal proliferation accompanied by reduced cell death with the ability to survive under stresses of nutrient and growth factor deprivation, hypoxia, and loss of cell-to-cell contacts. At the molecular level, cancer is a genetic disease that develops due to the accumulation of mutations over time in somatic cells. The phenotype includes genomic instability and chromosomal aneuploidy that allows for acceleration of genetic change. Malignant transformation and tumor progression of any cell requires immortalization, loss of checkpoint control, deregulation of growth, and survival. A tremendous amount has been learned about the numerous cellular and molecular genetic changes and the host-tumor interactions that accompany tumor development and progression. It is the goal of the field of Molecular Oncology to use this knowledge to understand cancer pathogenesis and drug action, as well as to develop more effective diagnostic and therapeutic strategies for cancer. This includes preventative strategies as well as approaches to treat metastases. With the availability of the human genome sequence and genomic and proteomic approaches, a wealth of tools and resources are generating even more information. The challenge will be to make biological sense out of the information, to develop appropriate models and hypotheses and to translate information for the clinicians and the benefit of their patients. Cancer Biology & Therapy aims to publish original research on the molecular basis of cancer, including articles with translational relevance to diagnosis or therapy. We will include timely reviews covering the broad scope of the journal. The journal will also publish op-ed pieces and meeting reports of interest. The goal is to foster communication and rapid exchange of information through timely publication of important results using traditional as well as electronic formats. The journal and the outstanding Editorial Board will strive to maintain the highest standards for excellence in all activities to generate a valuable resource.
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