| Target gene or protein |
c-Myc, Cyclin D1, Bcl-2, ABCB1, ABCC1, ABCG2, CXCL1, CXCL2, CXCR4, PTEN, BMI1, EGFR, CRP, EZH2, FABP5, ABCB4, DYRK2, HR.SERPINE1, PGAP3, MAP3K1, MAPK1, TCF, MTOR, AKT1, BIRC5, CCND1 , NQO1, PRMT5, MEP50, AURKA, CDK2, CDK1, FOS, H2AX, KIF11, SOD2, STAT-3, TNF, APC, ARNT,AXIN1, HIAP1, CRAF1, TRAF6, CASP1, CASP2, CASP3, CASP4, HPRT, GADD45, MCL-1, NIP1, Bcl-2L2, TRAP3, GSTP1, DAXX, PIG11, UBC, PIG3, PCNA, CDC10, JNK1, RBP2, TRAIL, TNFR, AP13, IGFBP3, SARP3, PKB, IGFBP, CASP7, CASP9, TNFSF6, TRICK2A, CAS, TRAIL-R2, RATS1, hTRIP, TNFb, TNFRSF5, CASP9, COL4A1, DAXX, DVL2, ENPP2, ERP29, FASN, ISG15, MYBL1 , PDK1, VEGF-A, XIAP, PARP, HER-2, NF-kB, Caspase 3, Caspase 7, skp2, p27, Cadherin-11, Plasminogen |
| Gene or Protein evidence |
The knockdown of RPS3 inhibited cell growth and induced apoptosis as well as the downregulation of XIAP in breast cancer cells.
In combination with quercetin, Causes down-regulation of Wnt/β-catenin signaling pathway proteins, DVL2, β-catenin, cyclin D1, Cox2, and Axin2 and down-regulation of BCL2 and induction of caspase 3/7 through PARP cleavage (A375 cells).
Reverses BPA-induced upregulation of oncogenic miR-19a and miR-19b, and the dysregulated expression of miR-19-related downstream proteins, including PTEN, p-AKT, p-MDM2, p53, and proliferating cell nuclear antigen.
The up-regulated genes include HIAP1, CRAF1, TRAF6, CASP1, CASP2, CASP3, CASP4, HPRT, GADD45, MCL-1, NIP1, BCL2L2, TRAP3, GSTP1, DAXX, PIG11, UBC, PIG3, PCNA, CDC10, JNK1 and RBP2. The down-regulated genes were TRAIL, TNFR, AP13, IGFBP3, SARP3, PKB, IGFBP, CASP7, CASP9, TNFSF6, TRICK2A, CAS, TRAIL-R2, RATS1, hTRIP, TNFb and TNFRSF5.
In order to elucidate the mechanisms responsible for the overexpression of the XIAP protein in breast cancer, we attempted to clarify the mechanisms by which the natural compound curcumin downregulates XIAP in breast cancer cells.
Taken together, these results suggest that nontoxic synthetic curcumin analogs with increased bioavailability, especially GO-Y030 and GO-Y078, inhibit the function of ABCG2 by directly interacting at the substrate-binding site.
Curcumin also directly reduces HR and induces cell death with cotreatment of PARP inhibitor in MDA-MB-231 breast cancer cells.
Knowing that curcumin has been used as food to inhibit cancer activity, this study evaluated the efficacy of natural curcumins and curcumin analogs as HER2 inhibitors using in vitro and in silico studies.
All compounds except resveratrol induced caspase 3/7 dependent apoptosis.
Multicolor bioluminescence in vivo imaging allowed the investigation of tumor growth and NF-κB induction in a mouse model of breast cancer.
Further, we found that quercetin and curcumin induced growth arrest by inhibition of Skp2, and induced p27 expression in MDA-MB-231 cells.
DIM and curcumin decreased cadherin-11 and increased urokinase-type plasminogen activator levels correlated with increased cell motility. |
| Additional information |
Suppresses retinoic acid-induced PPARβ/δ target gene, VEGF-A
Induces G2/M phase cell cycle arrest and apoptosis, causes decrease of CDC25 and CDC2 and increase of P21 protein levels, as well as inhibition of the phosphorylation of Akt/mTOR, inhibits the generation of reactive oxygen species (ROS)
In combination with quercetin, Causes down-regulation of Wnt/β-catenin signaling pathway proteins, DVL2, β-catenin, cyclin D1, Cox2, and Axin2 and down-regulation of BCL2 and induction of caspase 3/7 through PARP cleavage (A375 cells)
Curcumin analogs with increased bioavailability, especially GO-Y030 and GO-Y078, inhibit the function of ABCG2
Downregulates the inflammatory cytokines CXCL1 and -2 in breast cancer cells via NFkappaB
Reverses BPA-induced upregulation of oncogenic miR-19a and miR-19b, and the dysregulated expression of miR-19-related downstream proteins, including PTEN, p-AKT, p-MDM2, p53, and proliferating cell nuclear antigen
Reverses doxorubicin resistance by inhibiting the ATPase activity of ABCB4 (MCF‑7/DOX and MDA‑MB‑231/DOX cells)
Reduces tumor burden in immunocompromised mice, showing a similar antitumor effect as CRISPR/Cas9-mediated DYRK2 depletion (breast cancer xenograft model).
9.
Phase II Study of Curcumin vs Placebo for Chemotherapy-Treated Breast Cancer Patients Undergoing Radiotherapy
"Curcumin" in Combination With Chemotherapy in Advanced Breast Cancer |