Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5506830 | Biochemical and Biophysical Research Communications | 2016 | 8 Pages |
Abstract
To investigate the effects of CYP4Z1 3â²UTR in migration of breast cancer cells, a series of assays were used to confirm that overexpression of CYP4Z1 3â²UTR could suppress the capacity of migration and adhesion of MCF-7 and MDA-MB-231Â cells. EMT (Epithelial-mesenchymal transition)-related proteins were regulated by CYP4Z1 3â²UTR. Mesenchyma markers like Vimentin, MMP-2, and MMP-9 were down-regulated, while the expression of E-cadherin was up-regulated with CYP4Z1 3â²UTR overexpression. Notably, luciferase reporter and qRT-PCR assays were applied to verify that CYP4Z1 3â²UTR was the potential target of miR-9. In addition, our results showed that CYP4Z1 3â²UTR 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 3â²UTR could inhibit the migration and EMT of breast cancer cells via acting as a ceRNA for E-cadherin.
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Authors
Bingyu Wang, Lufeng Zheng, Jinjiang Chou, Cheng Li, Yan Zhang, Xia Meng, Tao Xi,