Chloroquine (CQ) exerts anti-breast cancer through modulating microenvironment and inducing apoptosis

CQ is an anti-malaria drug, which has been used for years. However, there are published articles about its activity in anti-cancers. The aim of this approach was to look at possibility and related mechanisms of anti-breast cancer (mouse breast cancer cell line 4T1) by CQ alone. The studies of anti 4...

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Veröffentlicht in:International immunopharmacology 2017-01, Vol.42, p.100-107
Hauptverfasser: Zhang, Yanjun, Cao, Yu, Sun, Xiaodan, Feng, Yonghui, Du, Yunting, Liu, Fei, Yu, Chunyun, Jin, Feng
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Sprache:eng
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Zusammenfassung:CQ is an anti-malaria drug, which has been used for years. However, there are published articles about its activity in anti-cancers. The aim of this approach was to look at possibility and related mechanisms of anti-breast cancer (mouse breast cancer cell line 4T1) by CQ alone. The studies of anti 4T1 in vitro and in vivo by CQ were performed. The growth of 4T1 in vitro and in vivo, survival of mice post treatment with CQ, changes of immune parameters and microenvironment in mice were evaluated. Our results demonstrate that CQ could markedly inhibit growth of 4T1 in vitro through inducing apoptosis of cells, inhibiting secretion of TGF-β and prolong the mice survival in vivo through boosting immune system by upregulating CD8+ T cell, and through down-regulating tumor associated macrophages (TAM), myeloid derived suppressing cells (MDSC) and Tregs, in microenvironment of mice bearing tumor. This provides a new mode of action for CQ and it is therefore concluded that CQ could be with potential in breast cancer therapy. •CQ could markedly inhibit growth of 4T1 in vitro through inducing apoptosis of cells, inhibiting secretion of TGF-β.•CQ could prolong the mice survival in vivo through boosting immune system by upregulating CD4+Th1, CD8+T cell, and IFN-γ secretion.•CQ could inhibit tumor growth through down-regulating TAM, MDSC and Tregs, in microenvironment of mice bearing tumor.
ISSN:1567-5769
1878-1705
DOI:10.1016/j.intimp.2016.11.027