WSTF Modulates Migration of Breast Cancer through Regulating Expressions of p21 and CCL2
Keywords:
WSTF, breast cancer, migration, p21, CCL2Abstract
Background: The purpose of this study is to investigate the regulation of Williams syndrome transcription factor (WSTF) on the migration ability of breast cancer cells, as well as whether cyclin-dependent kinase inhibitor 1A (p21) and C-C Motif Chemokine Ligand 2 (CCL2) genes are involved in.
Methods: Quantitative real-time PCR (qRT-PCR) and Immunohistochemistry (IHC) were used to test gene expression in breast cell lines and tissues, respectively. Western blotting was used to test protein expression. SiRNAs were transfected to knockdown WSTF to verify its functions. Transwell assay was used for migration determination.
Results: In our research, we found that WSTF was upregulated in breast cancer cells and tissues, compared to adjacent normal controls. Knockdown of WSTF markedly suppressed migration abilities of MDA-MB-231 and MCF-7 cells. Rescue assays illustrated that overexpression of p21 and CCL2 reversed the inhibition effect of WSTF knockdown on migration ability of breast cancer cells.
Conclusion: These findings revealed that hyper-expressed WSTF in breast cancer promoted the cell migration ability by upregulating p21 and CCL2 expressions.
