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. 2013 Jun;16(2):133-7.
doi: 10.4048/jbc.2013.16.2.133. Epub 2013 Jun 28.

The effect of curcumin on breast cancer cells

Dongwu Liu  1 , Zhiwei Chen
Affiliations

The effect of curcumin on breast cancer cells

Dongwu Liu et al. J Breast Cancer. 2013 Jun.

Abstract

Curcumin, which is extracted from the plant Curcuma longa, has been used in the therapeutic arsenal for clinical oncology. Curcumin has chemopreventive and antitumoral activities against some aggressive and recurrent cancers. The expressions and activities of various proteins, such as inflammatory cytokines and enzymes, transcription factors, and gene-products linked with cell survivals and proliferation, can be modified by curcumin. Moreover, curcumin decreases the toxic effect of mitomycin C. Though curcumin has shown highly cytotoxic to some cancer cell lines, curcumin is insoluble and instable in water. The solubility of curcumin could be enhanced by utilizing the solubilizing properties of rubusoside. In addition, the selective delivery of synthetic analogs or nanotechnology-based formulations of curcumin to tumors may improve the chemopreventive and chemotherapeutic effects. The focus of this short review is to describe how curcumin participates in antitumor processes in breast cancer cells.

Keywords: Breast neoplasms; Curcumin; Mitomycin C; Molecular mechanisms of pharmacological action.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Figure 1
Figure 1
The chemical structure of curcumin.
Figure 2
Figure 2
Curcumin inhibits the expression of zeste homologue 2 (EZH2) gene, AIP-1/Alix protein, Ki-67, proiferating cell nuclear antigen (PCNA), Bcl-2, and genes related to Wnt/β-catenin signaling pathway in cancer cells, but induces the expression of maspin and Bax in cancer cells. JNK=c-Jun NH2-terminal kinase; ERK=extracellular signal-regulated kinase.
Figure 3
Figure 3
Curcumin inhibits the expression of recepteur d'origine nantais (RON), human epidermal growth factor 2 (HER2), Akt, mitogen-activated protein kinase (MAPK), nuclear factor-κB (NF-κB), vascular endothelial growth factor (VEGF) and the phosphorylation of Src and stat3 through PRL-3 down-regulation, but induces the expression of p27 and poly (ADP-ribose) polymerase 1 (PARP-1) in cancer cells.
Figure 4
Figure 4
The chemical structure of mitomycin C.
Figure 5
Figure 5
Mitomycin C and curcumin combination treatment inhibits the expression of glucose regulatory protein (GRP58), cyclin D1, cyclin E, cyclin A, cyclin-dependent kinase 2 (CDK2), and CDK4, but induces the expression of p21 and p27 in cancer cells.
See this image and copyright information in PMC

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