Work

PRRX1 drives tamoxifen therapy resistance through induction of epithelial-mesenchymal transition in MCF-7 breast cancer cells.

Year: 2018
Type: article
Abstract: PURPOSE: using ER-positive MCF-7 breast cancer cells. METHODS: PRRX1 was overexpressed in MCF-7 cells through transfection; cells transfected with a blank vector served as the control. The morphological changes and transfection efficiency were observed by inverted fluorescence microscopy. The expression of ER and EMT-related proteins and genes was evaluated by Western blot and real-time polymerase chain reaction analysis, respectively. Finally, we evaluated the EMT features of the breast cancer cells and their response to TAM treatment. RESULTS: and vimentin were significantly higher, whereas that of E-cadherin was significantly lower after transfection. The proliferative level of the breast cancer cells after transfection was significantly increased at 12, 24 and 48 h after treatment with TAM. At 24 h of TAM treatment, the half-maximal inhibitory concentration of the transfected cells was significantly higher than that before transfection. Moreover, the PRRX1-overexpressing MCF-7 breast cancer cells acquired an EMT phenotype and displayed decreased levels of ER targets to ultimately acquire resistance to TAM. CONCLUSIONS: PRRX1 overexpression can induce EMT to promote resistance to TAM in MCF-7 breast cancer cells, partly by reducing ER expression. It is suggested that in clinical practice, PRRX1 gene expression detection can be performed in patients with hormone-receptor-positive breast cancer to guide our medication and prognosis.
Language: English
Subfield: Oncology
Field: Medicine
Open Access status: green
OpenAlex ID: W3011858851
FWCI: 0.209
Cites: 22
Cited by: 6
Related to: 10