Inhibition of microRNA-660-5p decreases breast cancer progression through direct targeting of TMEM41B.

IF 2.7 3区 生物学
Valeria Villarreal-García, José Roberto Estupiñan-Jiménez, Vianey Gonzalez-Villasana, Pablo E Vivas-Mejía, Marienid Flores-Colón, Irma Estefanía Ancira-Moreno, Patricio Adrián Zapata-Morín, Claudia Altamirano-Torres, José Manuel Vázquez-Guillen, Cristina Rodríguez-Padilla, Recep Bayraktar, Mohamed H Rashed, Cristina Ivan, Gabriel Lopez-Berestein, Diana Reséndez-Pérez
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引用次数: 0

Abstract

Background: Breast cancer is the most prevalent cancer among women worldwide. Most breast cancer-related deaths result from metastasis and drug resistance. Novel therapies are imperative for targeting metastatic and drug-resistant breast cancer cells. Accumulating evidence suggests that dysregulated microRNAs (miRNAs) promote breast cancer progression, metastasis, and drug resistance. Compared with healthy breast tissue, miR-660-5p is notably overexpressed in breast cancer tumor tissues. However, the downstream effectors of miR-660-5p in breast cancer cells have not been fully elucidated. Our aim was to investigate the role of miR-660-5p in breast cancer cell proliferation, migration, invasion, and angiogenesis and to identify its potential targets.

Results: Our findings revealed significant upregulation of miR-660-5p in MDA-MB-231 and MCF-7 cells compared with MCF-10 A cells. Furthermore, inhibiting miR-660-5p led to notable decreases in the proliferation, migration, and invasion of breast cancer cells, as well as angiogenesis, in HUVEC cells. Through bioinformatics analysis, we identified 15 potential targets of miR-660-5p. We validated TMEM41B as a direct target of miR-660-5p via Western blot and dual-luciferase reporter assays.

Conclusions: Our study highlights the upregulation and involvement of miR-660-5p in breast cancer cell proliferation, migration, invasion, and angiogenesis. Additionally, we identified TMEM41B as a direct target of miR-660-5p in breast cancer cells.

通过直接靶向TMEM41B抑制microRNA-660-5p可减少乳腺癌进展。
背景:乳腺癌是世界范围内最常见的女性癌症。大多数乳腺癌相关死亡是由于转移和耐药性。针对转移性和耐药乳腺癌细胞的新疗法势在必行。越来越多的证据表明,失调的microRNAs (miRNAs)促进乳腺癌的进展、转移和耐药。与健康乳腺组织相比,miR-660-5p在乳腺癌肿瘤组织中明显过表达。然而,miR-660-5p在乳腺癌细胞中的下游效应尚未完全阐明。我们的目的是研究miR-660-5p在乳腺癌细胞增殖、迁移、侵袭和血管生成中的作用,并确定其潜在靶点。结果:我们的研究结果显示,与mcf - 10a细胞相比,MDA-MB-231和MCF-7细胞中miR-660-5p显著上调。此外,抑制miR-660-5p可显著降低乳腺癌细胞在HUVEC细胞中的增殖、迁移和侵袭以及血管生成。通过生物信息学分析,我们确定了miR-660-5p的15个潜在靶点。我们通过Western blot和双荧光素酶报告基因检测验证了TMEM41B是miR-660-5p的直接靶点。结论:我们的研究强调了miR-660-5p在乳腺癌细胞增殖、迁移、侵袭和血管生成中的上调和参与。此外,我们发现TMEM41B是乳腺癌细胞中miR-660-5p的直接靶点。
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
Hereditas Biochemistry, Genetics and Molecular Biology-Genetics
CiteScore
3.80
自引率
3.70%
发文量
0
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.
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