CircRNA-14052 promotes breast cancer progression via miR-214-3p/IKBKB pathway.

IF 2.5 3区生物学

Hereditas Pub Date : 2025-10-03 DOI:10.1186/s41065-025-00566-6

Donghai Li, Zhiying Zhang, Yan Cui, Jiaxin Sun, Wenyuan Wei, Shaofeng Yang, Rui Zhang

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引用次数: 0

Abstract

Objectives: Circular RNAs play crucial regulatory roles in the progression of human diseases. This study aimed to investigate the functional mechanism of circRNA-14,052 in breast cancer progression.

Methods: The biological functions of circRNA-14,052 were assessed using CCK-8, wound healing, flow cytometry assays. The ceRNA regulatory network of circRNA-14,052-miR-214-3p- IKBKB was validated by luciferase reporter assay.

Results: The levels of circRNA-14,052 were notably elevated, but the levels of miR-214-3p were markedly reduced in breast cancer tissues compared to adjacent non-cancerous tissues. Downregulation of circRNA-14,052 or overexpression of miR-214-3p reduced MCF-7 cell proliferation and triggered cell apoptosis. Mechanically, circRNA-14,052 could elevate IKBKB levels via competitively sponging miR-214-3p. Notably, miR-214-3p inhibition reversed the growth-suppressive effects of circRNA-14,052 silencing. Additionally, circRNA-14,052 knockdown notably reduced IKBKB, IL-6, JAK2 and STAT3 levels in MCF-7 cells; whereas these changes were reversed by miR-214-3p deficiency. Furthermore, deficiency of circRNA-14,052 reduced xenograft tumor growth in vivo through targeting miR-214-3p/IKBKB/IL-6/JAK2/STAT3 axis.

Conclusion: Collectively, our results showed that circRNA-14,052 promotes breast cancer progression via the miR-214-3p/IKBKB axis. Targeting this molecular axis may represent a promising therapeutic strategy for breast cancer treatment.

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CircRNA-14052通过miR-214-3p/IKBKB途径促进乳腺癌进展。

目的：环状rna在人类疾病的进展中起着至关重要的调节作用。本研究旨在探讨circrna - 14052在乳腺癌进展中的作用机制。方法：采用CCK-8、创面愈合、流式细胞术等方法评价circrna - 14052的生物学功能。荧光素酶报告基因试验验证了circRNA-14,052-miR-214-3p- IKBKB的ceRNA调控网络。结果：乳腺癌组织中circrna - 14052水平明显升高，miR-214-3p水平明显低于癌旁非癌组织。下调circrna - 14052或过表达miR-214-3p可降低MCF-7细胞增殖并引发细胞凋亡。机械地，circrna - 14052可以通过竞争性海绵miR-214-3p提高IKBKB水平。值得注意的是，miR-214-3p抑制逆转了circrna - 14052沉默的生长抑制作用。此外，circrna - 14052敲低显著降低了MCF-7细胞中的IKBKB、IL-6、JAK2和STAT3水平；而这些变化被miR-214-3p缺失逆转。此外，circrna - 14052的缺失通过靶向miR-214-3p/IKBKB/IL-6/JAK2/STAT3轴，在体内降低了异种移植物肿瘤的生长。结论：总的来说，我们的研究结果表明circrna - 14052通过miR-214-3p/IKBKB轴促进乳腺癌进展。靶向这一分子轴可能是一种很有前途的乳腺癌治疗策略。

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

Hereditas Biochemistry, Genetics and Molecular Biology-Genetics

CiteScore

3.80

自引率

3.70%

发文量

期刊介绍： For almost a century, Hereditas has published original cutting-edge research and reviews. As the Official journal of the Mendelian Society of Lund, the journal welcomes research from across all areas of genetics and genomics. Topics of interest include human and medical genetics, animal and plant genetics, microbial genetics, agriculture and bioinformatics.