Abstract
BackgroundThe role of epithelial–mesenchymal transition (EMT) involved in breast cancer metastasis and chemoresistance has been increasingly recognized. However, it is necessary to search for more effective strategies to inhibit EMT thereby increase the sensitivity of breast cancer cells to chemotherapy drugs. Emodin has a potential in overcoming tumor drug resistance and restraining the development of EMT, but the poor internalization into breast cancer cells limited the application.ResultsMCF-7/ADR cells have more EMT characteristics than MCF-7 cell. EMT in MCF-7/ADR cells promotes the development of drug resistance via apoptosis resistance and facilitating the expression of P-gp. The anti-cancer effect of DOX enhanced by the decreasing of drug resistance protein P-gp and apoptosis-related proteins after EMT inhibited in MCF-7/ADR cells. E-PLNs increase the cellular uptake of EMO and restore DOX sensitivity in MCF-7/ADR cells by inhibiting EMT.ConclusionE-PLNs inhibit EMT to enhance the sensitivity of breast cancer to DOX. The combination of E-PLNs and DOX can improve the efficacy of DOX in the treatment of breast cancer, which provides a new method to prevent or delay clinical drug resistance.
Highlights
The role of epithelial–mesenchymal transition (EMT) involved in breast cancer metastasis and chemoresistance has been increasingly recognized
Compared with DOX group, the number of invasive cells in DOX + EMO (30 μM) group and DOX + Emodin-loaded polymer-lipid hybrid nanoparticles (E-Polymeric lipid nanoparticles (PLNs)) (30 μM) group decreased, and DOX + E-PLNs group was more significant. These results shown that the combination of E-PLNs and DOX can inhibit the occurrence of EMT and the tendency to invasion in MCF-7/ADR cells
We find that appears MCF-7/ADR cells have more significant characteristics of EMT than DOX sensitive MCF-7 cells, manifested as the down-regulated of E-cadherin protein and the Transforming growth factor beta (TGF-β) signaling plays a key role in epithelial-mesenchymal transition (EMT) of tumors (Xu et al 2009)
Summary
The role of epithelial–mesenchymal transition (EMT) involved in breast cancer metastasis and chemoresistance has been increasingly recognized. Emodin has a potential in overcoming tumor drug resistance and restraining the development of EMT, but the poor internalization into breast cancer cells limited the application. EMO has a potential in overcoming tumor drug resistance and restraining the development of EMT (Liu et al 2020a, b; Fu et al 2012; Lu et al 2016; Gu et al 2019) It can effectively increase the accumulation of doxorubicin (DOX) by downregulating the expression of P-gp in lung adenocarcinoma and colorectal carcinoma cells (Iyer et al 2018).
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