Table 1.
Therapeutic approaches using sulforaphane for treating different tumors and its effects.
| Therapy | Cancer Type | Affected Cancer Cell Population | Model | Effects | References |
|---|---|---|---|---|---|
| SFN | Prostate Cancer | CSCs | Men on active surveillance for prostate cancer | Dose-dependent inhibition of oncogenic pathways such as TGF-β, Kras, NFκ-B, and Notch. | 78 |
| SFN | Pancreatic Cancer | CSCs | PANC-1, MIA PaCa-2, AsPC-1 and Bx PC-3 human cell lines | Reduction of EMT-related genes expression including β-catenin, vimentin, Twist-1, and Zeb-1. | 74 |
| SFN + DOX | Mammary Adenocarcinoma | Non-CSCs | MATB-III rat mammary gland tumor cell line, Sprague Dawley rats; 4T1 murine cell line, Balb/C mice | Inhibition of tumor growth with lower DOX dosage, reduced cardiotoxicity upon activation of Nrf2; Reduction in tumor volume, increase in cytotoxic CD8+T cells, decrease in MDSC population with subsequent immunosuppression. | 20, 79 |
| SFN + Nano-metformin | Breast Cancer | CSCs | MCF-10, MCF-7, and BT-474 human cell lines | Decrease in Wnt1, β-catenin and CD44 expression; While increased Bax expression and cell death. | 80 |
| SFN + Quercetin | Pancreatic Cancer | CSCs | PANC-1, MIA PaCa-2, AsPC-1 and Bx PC-3 human cell lines | Higher inhibition of self-renewal capacity of PCSCs. | 74 |
| SFN + CIS/DOX/GEM/5-flurouracil | Pancreatic Cancer | CSCs | MIA-PaCa2 and DU145 human cell lines Balb/C nude mice |
Anti-proliferative effects; Abolishment of tumor initiation capacity. | 81 |
| SFN + Curcumin/dihydrocaffeic acid | Colon Cancer | Non-CSCs | Caco-2 and HT-29 human cell lines | Combination-dependent cytotoxic effects. | 77 |
SFN, Sulforaphane; DOX, Doxorubicin; CSCs, Cancer Stem Cells; MDSC, Myeloid-Derived Suppressor Cell; EMT, Epithelial-to-Mesenchymal Transition; CIS, Cisplatin; GEM, Gemcitabine.