Li Xin, Liu Jie, He Lili, Tian Mi, Xu Yingying, Peng Bing
Department of Thyroid and Breast, Jingmen City People's Hospital, Jingmen, Hubei, P.R. China.
Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Universiti Malaysia Sabah, Jalan UMS, 88400, Kota Kinabalu, Sabah, Malaysia.
Protein Pept Lett. 2025;32(3):171-182. doi: 10.2174/0109298665339026250114070523.
Endogenous microRNAs (miRNAs) are critical regulators of tumor progression, making their role in breast cancer an important area of investigation.
This study examined the regulation of MSMO1 by miR-584-5p in breast cancer cells. Using bioinformatics and Western blotting, we confirmed MSMO1 expression in breast cancer cells and evaluated its effects on cell migration, invasion, and the AKT signaling pathway. In vivo experiments further supported these findings. The interaction between miR-584-5p and MSMO1 was validated through luciferase reporter assays, while functional studies highlighted the impact of miR-584-5p on cancer progression.
Our findings revealed that MSMO1 is upregulated in breast cancer, enhancing cell migration and invasion. Silencing MSMO1 diminished AKT pathway activity, and luciferase assays confirmed MSMO1 as a direct target of miR-584-5p.
Overexpression of miR-584-5p suppressed migration and invasion of breast cancer cells. In summary, miR-584-5p is likely to modulate MSMO1 and subsequently regulate the AKT/ PI3K pathway, presenting a promising therapeutic target for breast cancer treatment.
内源性微小RNA(miRNA)是肿瘤进展的关键调节因子,这使得它们在乳腺癌中的作用成为一个重要的研究领域。
本研究检测了miR-584-5p对乳腺癌细胞中MSMO1的调控作用。通过生物信息学和蛋白质免疫印迹法,我们证实了MSMO1在乳腺癌细胞中的表达,并评估了其对细胞迁移、侵袭及AKT信号通路的影响。体内实验进一步支持了这些发现。通过荧光素酶报告基因检测验证了miR-584-5p与MSMO1之间的相互作用,而功能研究突出了miR-584-5p对癌症进展的影响。
我们的研究结果显示,MSMO1在乳腺癌中上调,增强了细胞迁移和侵袭能力。沉默MSMO1可降低AKT通路活性,荧光素酶检测证实MSMO1是miR-584-5p的直接靶标。
miR-584-5p的过表达抑制了乳腺癌细胞的迁移和侵袭。总之,miR-584-5p可能调节MSMO1,进而调节AKT/PI3K通路,为乳腺癌治疗提供了一个有前景的治疗靶点。