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  • br Immunohistochemical staining revealed the

    2022-09-14

    
    Immunohistochemical staining revealed the abolished vimentin levels and increased E-cadherin levels in the tissues subjected to dual treat-ment. Overall, H2O2 was generated in CAP-treated A549 cancer U 46619 [59,60], while Fe2+/Fe3+ from iron oxide-based MNPs can transform H2O2 into •OH via Fenton’s reaction [61]. Iron oxide-based MNPs can enhance the tumor-killing effect of CAP through this mechanism (Fig. 10). These results suggested that dual treatment with CAPs and iron oxide-based MNPs potentially inhibited tumor growth.
    5. Conclusions
    In summary, the effect of co-treatment of CAP and iron oxide-based MNPs both in vitro and in vivo has been demonstrated. The co-treat-ment could effectively induce A549 cancer cells apoptosis in vitro via the inhibition of EGFR-RAS/ERK and EGFR-PI3K/AKT signaling path-ways and the modulation of EMT. The co-treatment also suppressed xenograft tumor growth. Thus, the combination of CAP and iron oxide-based MNPs may lead to a shift in the paradigm of cancer therapy.
    Acknowledgements
    This work was supported by a grant from the National Natural Science Foundation of China, China (81774125) and The Natural Science Foundation of Shandong Province, China (ZR2015HL064). The work at George Washington University was supported in part by National Science Foundation, USA (1465061).
    Authors contributions
    WL, ZC, MK, WZ: conception and design, data analysis and inter-pretation, and manuscript writing and revision; WL, ZC, HY, DD, YW, SW, XL: conduct experiments and data analysis. All authors have given approval to the final version of the manuscript
    Conflict of interest
    The authors declare no conflict of interest.
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    Fig. 10. Molecular mechanisms of MNPs enhancing tumor-selective killing effect of CAP. CAP-originated reactive species will cause a noticeable rise of in-tracellular H2O2, Fe2+/Fe3+ released from the lyso-some containing MNPs could catalyzed H2O2 into OH., which cause the injury of cancer cells, such as inducing mitochondria-mediated apoptosis and double strand DNA breaks.
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