Sulforaphene

The seeds of Brassica oleracea L. var. botrytis L.

Sulforaphene inhibits triple negative breast cancer through activating tumor suppressor Egr1.[Pubmed:27377973]

Breast Cancer Res Treat. 2016 Jul;158(2):277-86.

Sulforaphene (SFE, 4-methylsufinyl-3-butenyl isothiocyanate) is a member of isothiocyanates, which is derived from radish seeds. It has shown that multiple isothiocyanates, such as sulforaphane, can effectively inhibit cancer cell proliferation in vitro and in vivo. However, it is still largely unknown if SFE could impact breast cancer. In this study, we investigated the anticancer effects of SFE on triple negative breast cancer (TNBC) via a series of in vitro and in vivo assays. We found that SFE can significantly inhibit cell proliferation in multiple TNBC cell lines through inducing G2/M phase arrest as well as cell apoptosis. Nude mice xenograft assays support the anti-TNBC role of SFE in vivo. Interestingly, SFE can repress expression of cyclinB1, Cdc2, and phosphorylated Cdc2, and, then, induced G2/M phase arrest of TNBC cells. To identify SFE target genes, we detected genome-wide gene expression changes through gene expression profiling and observed 27 upregulated and 18 downregulated genes in MDA-MB-453 cells treated with SFE. Among these genes, Egr1 was successfully validated as a consistently activated gene after SFE treatment in TNBC MDA-MB-453 and MDA-MB-436 cells. Egr1 overexpression inhibited proliferation of TNBC cells. However, Egr1 knockdown using siRNAs significantly promoted TNBC cell growth, indicating the tumor suppressor nature of Egr1. In sum, we for the first time found that SFE might be a potential anti-TNBC natural compound and its antiproliferation effects might be mediated by tumor suppressor Egr1.

Sulforaphene enhances radiosensitivity of hepatocellular carcinoma through suppression of the NF-kappaB pathway.[Pubmed:28346727]

J Biochem Mol Toxicol. 2017 Aug;31(8).

Sulforaphene (SFE), a naturally occurring isothiocyanate found in cruciferous vegetables, has attracted increasing attention for its anti-cancer effect in many cancers, including hepatocellular carcinoma (HCC). However, the precise role of SFE in the radiosensitivity of HCC is still unclear. Here, cell proliferation and apoptosis were detected by MTT and flow cytometry assay, respectively. The activity of NF-kappaB was further evaluated by ELISA. We also observed the effect of SFE and/or radiation on tumor growth. The results showed that SFE inhibited cell proliferation and induced apoptosis in HCC cells. Radiation increased NF-kB activity, while PDTC, a NF-kB inhibitor, enhanced radiation-induced cell death. SFE inhibited NF-kB activity and the downstream gene expressions of the NF-kB pathway in HCC cells. Moreover, SFE enhanced the inhibitory effect of radiation on tumor growth both in vitro and in vivo. This study indicated that SFE sensitized the radiosensitivity of HCC by blocking the NF-kB pathway.

Herbicidal activity of sulforaphene from stock (Matthiola incana).[Pubmed:24248575]

J Chem Ecol. 1993 Oct;19(10):2279-84.

A herbicidal compound was isolated from extracts ofMatthiola incana and identified as Sulforaphene (4-methylsulfinyl-3-butenyl isothiocyanate). The ED50 of this compound against velvetleaf seedlings was approximately 2x10(-4) M. Glucoraphenin, the glucosinolate that is the natural precursor of Sulforaphene, was less phytotoxic, with an ED50 of near 6x10(-3)M.

Sulforaphene promotes Bax/Bcl2, MAPK-dependent human gastric cancer AGS cells apoptosis and inhibits migration via EGFR, p-ERK1/2 down-regulation.[Pubmed:26612919]

Gen Physiol Biophys. 2016 Jan;35(1):25-34.

Gastric cancer migration and invasion considered as main causes of this cancer-related death around the world. Sulforaphene (4-isothiocyanato-4R-(methylsulfinyl)-1-butene), a structural analog of sulforaphane, has been found to exhibit anticancer potential against different cancers. Our aim was to investigate whether dietary isothiocyanate Sulforaphene (SFE) can promote human gastric cancer (AGS) cells apoptosis and inhibit migration. Cells were treated with various concentrations of SFE and cell viability, morphology, intracellular ROS, migration and different signaling protein expressions were investigated. The results indicate that SFE decreases AGS cell viability and induces apoptosis in a dose-dependent manner. Intracellular ROS generation, dose- and time-dependent Bax/Bcl2 alteration and signaling proteins like cytochrome c, Casp-3, Casp-8 and PARP-1 higher expression demonstrated the SFE-induced apoptotic pathway in AGS cells. Again, SFE induced apoptosis also accompanied by the phosphorylation of mitogen-activated protein kinases (MAPKs) like JNK and P-38. Moreover, dose-dependent EGFR, p-ERK1/2 down-regulation and cell migration inhibition at non-toxic concentration confirms SFE activity in AGS cell migration inhibition. Thus, this study demonstrated effective chemotherapeutic potential of SFE by inducing apoptisis as well as inhibiting migration and their preliminary mechanism for human gastric cancer management.

Sulforaphene, isolated from radish seeds, exhibits an ED50 against velvetleaf seedlings approximately 2 x 10-4 M. Sulforaphene promotes cancer cells apoptosis and inhibits migration via inhibiting EGFR, p-ERK1/2, NF‐κB and other signals.

Sulforaphene,592-95-0,Natural Products, buy Sulforaphene , Sulforaphene supplier , purchase Sulforaphene , Sulforaphene cost , Sulforaphene manufacturer , order Sulforaphene , high purity Sulforaphene