Journal
MOLECULAR THERAPY-NUCLEIC ACIDS
Volume 16, Issue -, Pages 519-530Publisher
CELL PRESS
DOI: 10.1016/j.omtn.2019.04.006
Keywords
-
Categories
Funding
- Natural Science Foundation of China [NSFC81872587, NSFC81702530, NSFC81601849, NSFC81773391]
- Wenzhou Science and Technology Bureau [Y20170028, Y20160075, Y20180109]
- Zhejiang Medical and Health Science and Technology Project [2019RC217]
- Key Discipline of Zhejiang Province in Medical Technology
- Key Project of Science and Technology Innovation Team of Zhejiang Province [2013TD10]
- Xinmiao Talent Program of Zhejiang Province [2018R413068]
Ask authors/readers for more resources
Although microRNAs (miRNAs) are well-known for their potential in cancer, the function and mechanisms of miR-3648 have barely been explored in any type of cancer. We show here that miR-3648 is upregulated in human BC tissues in comparison with adjacent non-tumor tissues. Functional studies showed that inhibition of miR-3648 expression in the human invasive BC UMUC3 and T24T cell lines decreased migration and invasion in vitro and suppressed lung metastasis in vivo, whereas miR-3648 overexpression promoted BC cell migration and invasion. A bioinformatics screen and mRNA 3' UTR luciferase reporter assay showed that transcription factor 21 (TCF21) was a direct target of miR-3648, and the results obtained from using a miR-3648 inhibitor revealed that miR-3648 inhibited TCF21 protein expression by reduction of its mRNA stability. Further, Kisspeptin 1 (KISS1) was identified as a TCF21 downstream effector responsible for miR-3648-mediated BC invasion and lung metastasis. Collectively, the present results suggest that miR-3648 is overexpressed and plays an oncogenic role in mediation of BC invasion and metastasis through directing the TCF21/KISS1 axis, revealing miR-3648 as a potential biomarker for BC prognosis and a target for BC therapy.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available