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CYP4Z1 3′UTR represses migration of human breast cancer cells
- Source :
- Biochemical and Biophysical Research Communications. 478:900-907
- Publication Year :
- 2016
- Publisher :
- Elsevier BV, 2016.
-
Abstract
- To investigate the effects of CYP4Z1 3′UTR in migration of breast cancer cells, a series of assays were used to confirm that overexpression of CYP4Z1 3′UTR could suppress the capacity of migration and adhesion of MCF-7 and MDA-MB-231 cells. EMT (Epithelial-mesenchymal transition)-related proteins were regulated by CYP4Z1 3′UTR. Mesenchyma markers like Vimentin, MMP-2, and MMP-9 were down-regulated, while the expression of E-cadherin was up-regulated with CYP4Z1 3′UTR overexpression. Notably, luciferase reporter and qRT-PCR assays were applied to verify that CYP4Z1 3′UTR was the potential target of miR-9. In addition, our results showed that CYP4Z1 3′UTR repressed the expression of E-cadherin in a miRNA-dependent manner. Combining with our previous study, we have discovered the underlying link between CYP4Z1 and E-cadherin. Therefore, those preliminary data suggest that CYP4Z1 3′UTR could inhibit the migration and EMT of breast cancer cells via acting as a ceRNA for E-cadherin.
- Subjects :
- 0301 basic medicine
Epithelial-Mesenchymal Transition
Biophysics
Breast Neoplasms
Mesenchyma
Vimentin
Biology
Transfection
Bioinformatics
Biochemistry
03 medical and health sciences
0302 clinical medicine
Breast cancer
Antigens, CD
Cell Movement
Cell Line, Tumor
microRNA
Cell Adhesion
medicine
Humans
Cytochrome P450 Family 4
RNA, Small Interfering
3' Untranslated Regions
Molecular Biology
Transition (genetics)
Competing endogenous RNA
Three prime untranslated region
Cell Biology
Cadherins
medicine.disease
MicroRNAs
030104 developmental biology
030220 oncology & carcinogenesis
Cancer cell
Cancer research
biology.protein
Female
Subjects
Details
- ISSN :
- 0006291X
- Volume :
- 478
- Database :
- OpenAIRE
- Journal :
- Biochemical and Biophysical Research Communications
- Accession number :
- edsair.doi.dedup.....24478465ff7bffe2499c4447d7a93261
- Full Text :
- https://doi.org/10.1016/j.bbrc.2016.08.048