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Epithelial-mesenchymal transition modulates P-glucoprotein-induced multidrug resistance in breast cancer MCF-7 cells via p38-MAPK
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Abstract:
Abstract Objective:To investigate the relationship between epithelial-mesenchymal transition (EMT) and P-glucoprotein (P-gp)-induced multidrug resistance (MDR) in breast cancer cells and the corresponding mechanisms. Methods: Eukaryotic expression vector pcDNA-Snail was constructed and then transfected into human breast cancer cell line MCF-7. Multidrug resistance was induced by doxorubicin (DOX) in different groups. Expressions of epithelial marker E-cadherin, interstitial marker vimentin, and P-glucoprotein (P-gp) were detected by immunofluorescence. MTT assay was used to measure the proliferation of drug resistant MCF-7 cells. Expressions of Snail, MDR1, and p38-MAPK mRNA were evaluated by RT-PCR. Results: Immunofluorescence showed that MCF-7 cells had EMT after transfection with pcDNA-Snail vector. The expression of E-cadherin was downregulated, and expressions of vimentin and P-gp were upregulated in EMT-like MCF-7 cells. Drug resistance of MCF-7/Snail cells was significantly enhanced compared with MCF-7 cells after induction by DOX (P<0.05). The expressions of MDR1 and p38-MAPK mRNA in EMT-like cells were also significantly increased compared with those in parental MCF-7 cells (P<0.05). Conclusion: EMT may trigger DOX-induced and P-gp-mediated MDR via p38-MAPK in MCF-7 cells.
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Project Supported:
Project supported by the Natural Science Foundation of Shandong Province (No.Y2008C75)
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