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Table 1 Growth inhibitory effect of curcumin on breast cancer

From: Curcumin: the spicy modulator of breast carcinogenesis

Effect Curcumin alone or in combination Model used (*cell line/**animal) Expression phenotype of the cancer model Solubilization of curcumin Mechanism Reference
Suppression of cell proliferation & cell cycle regulation Curcumin *MCF7 ER+ PR+ Her2 Ethanol. Inhibits phosphorylation of mTOR and its downstream effector molecule p70S6K and eukaryotic initiation factor 4E (eIF4E) binding protein 1 (4E-BP1), [33]
Curcumin *MDA-MB-231 & BT-483 ER PR Her2 Dimethyl sulphoxide (DMSO) Down-regulation of NF-kB, cyclin D and MMP-1 transcription [40]
Curcumin *Breast cancer cells BALB-neuT
**BALB/c mice
Cancer cells expressing either high or low levels of ErbB2/neu. Description not available Down regulation of ERK1/ERK2 MAP kinases activity; dose dependant manner. [43]
Curcumin +Mitomycin C (MMC) *MCF-7
**MCF-7 xenograft Female nu/nu athymic mice
ER+ PR+ Her2 DMSO p38 MAPK pathway mediated inhibition of cyclin D1, cyclin E, cyclin A, CDK2 & CDK4 with induction of cell cycle inhibitor p21, and p27. [44]
Curcumin *MCF-7 & MDA-MB-231 ER+ PR+ Her2
ER PR Her2
DMSO Inhibit expression of Wnt/β-catenin pathway components: disheveled, beta-catenin, cyclin D1 and slug with alteration of GSK3beta and E-cadherin. [48]
Curcumin *MCF-7 ER+ PR+ Her2 DMSO Nrf2-mediated down-regulation of Fen1 expression; Nrf2 translocation from the cytoplasm to the nucleus and decrease Fen1 promoter activity by decreasing the recruitment of Nrf2 to the Fen1 promoter. [51]
Apoptosis Curcumin *MCF-7 ER+ PR+ Her2 Ethanol Concentration-dependent regulation of genes related to cell death. [53]
Curcumin *MCF 7, MDAH041 (post-crisis cell line from fibbroblasts of patient with LiFraumeni syndrome) & TR9-7 (derived from MDAH041 cells) ER+ PR+ Her2
the normal p53 allele has been lost during in vivo propagation.
TR9-7: express wild-type p53 under control of tetracycline-regulated promoter
Description not available Increase in p53 level & its DNA-binding activity followed by Bax expression at the protein level [55]
Curcumin *ENU1564
(originated from an N-ethyl-N nitosourea-induced mammary adenocarcinoma in a female Berlin-Druckrey IV rat)
  Description not available Via intrinsic mitochondrial pathway; increased mitochondrial Ca (2+) and reactive oxygen species production with increased mitochondrial permeability transition. [57]
Curcumin *MDA-MB-231 ER PR Her2 DMSO Dose-dependent inhibition of proliferation; increase Bax to Bcl-2 ratio; increases the protein level of p21 but decreases it for p53 [58]
Curcumin +citral *MCF 7 ER+ PR+ Her2
ER PR Her2
Description not available Cell cycle arrest in G0/G1 phase; induced high levels of reactive oxygen species (ROS) generation and activated p53 and poly (ADP-ribose) polymerase-1 mediated apoptotic pathways. [59]
Curcumin *MDA-MB-231 ER PR Her2 Description not available p53-Notch1 axis mediated downregulation of Notch1 and its downstream target, Hes1 [65]
Curcumin *MDA468 & HCC1806 ER PR Her2 Ethanol Induces double stranded DNA break in cancer cell; promotes phosphorylation of ATM/chk2-specific sites on BRCA1, total expression, and cytoplasmic retention of the BRCA1 protein; BRCA1 is retained in the cytoplasm where it cannot repair DNA damage; activates a DNA damage response in TNBC cells, leading to apoptosis [68]
Curcumin *MCF-7 ER+ PR+ Her2 DMSO Suppression of IGF-1R gene expression; down-regulate the IGF-1 axis with a decrease in secretion of IGF-1 with a concomitant increase of IGFBP-3 in a dose-dependent manner. [70]
Curcumin *MCF-7 ER+ PR+ Her2 DMSO Depolymerizes mitotic microtubules, disturbs microtubule-kinetochore attachment and the mitotic spindle structure. Activates the mitotic checkpoint and delays mitotic progression from metaphase to anaphase; p53 dependant apoptosis. [71]
Induction of senescence Curcumin+ silibin *T47D ER positive DMSO Decreases human telomerase reverse transcriptase (hTERT) gene expression [73]
Curcumin *Patient-derived primary breast CAF cells (bCAF)   DMSO p16-dependent, DNA damage independent; without associated inflammatory secretory phenotype [74]