Difference between sulforaphane and sulforaphene in colon cancer
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE174444 | GEO | 2021/05/15
REPOSITORIES: GEO
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Project description:Epidemiological studies provide strong evidence that consumption of cruciferous vegetables, such as broccoli, can significantly reduce the risk of developing cancers. Sulforaphane (SFN), a phytochemical derived from cruciferous vegetables, induces anti-proliferative and pro-apoptotic responses in prostate cancer cells, but not in normal prostate cells. The mechanisms responsible for these specific chemopreventive properties remain unclear. We utilized RNA sequencing to test the hypothesis that SFN modifies the expression of genes that are critical in prostate cancer progression. Normal prostate epithelial cells, and androgen-dependent and androgen-independent prostate cancer cells were treated with 15 µM SFN and the transcriptome was determined at 6 and 24 hour time points. SFN altered the expression of ~3,000 genes in each cell line and the response was highly dynamic over time. SFN influenced the expression of genes in functional groups and pathways that are critical in cancer including cell cycle, apoptosis and angiogenesis, but the specific effects of SFN differed depending on the state of cancer progression. Network analysis suggested that a transcription factor that is overexpressed in many cancers, Specificity protein 1 (Sp1), is a major mediator of SFN-induced changes in gene expression. Nuclear Sp1 protein was significantly decreased by 24 hour SFN treatment in prostate cancer cells, while a related transcription factor, Sp3 protein was only modestly decreased in androgen-independent prostate cancer cells. Overall, the data show that SFN significantly affects gene expression in normal and cancer cells, with key targets in chemopreventive processes, making it a promising dietary anti-cancer agent. Examination of how the transcriptome of normal and prostate cancer cells is altered by treatment with sulforaphane
2014-07-11 | E-GEOD-48812 | biostudies-arrayexpress
Project description:BACKGROUND. Prostate cancer is thought to arise as a result of oxidative stresses and induction of antioxidant electrophile defense (phase 2) enzymes has been proposed as a prostate cancer prevention strategy. The isothiocyanate sulforaphane, derived from cruciferous vegetables like broccoli, potently induces surrogate markers of phase 2 enzyme activity in prostate cells in vitro and in vivo. To better understand the temporal effects of sulforaphane and broccoli sprouts on gene expression in prostate cells, we carried out comprehensive transcriptome analysis using cDNA microarrays. METHODS. Transcripts significantly modulated by sulforaphane over time were identified using StepMiner analysis. Ingenuity Pathway Analysis (IPA) was used to identify biological pathways, networks, and functions significantly altered by sulforaphane treatment. . StepMiner and IPA revealed significant changes in many transcripts associated with cell growth and cell cycle, as well as a significant number associated with cellular response to oxidative damage and stress. Comparison to an existing dataset suggested that sulforaphane blocked cell growth by inducing G2/M arrest. Cell growth assays and flow cytometry analysis confirmed that sulforaphane inhibited cell growth and induced cell cycle arrest. CONCLUSIONS. Our data suggest that in prostate cells sulforaphane primarily induces cellular defenses and inhibits cell growth by causingG2/Mphase arrest. Furthermore, based on the striking similarities in the gene expression patterns induced across experiments in these cells, sulforaphane appears to be the primary bioactive compound present in broccoli sprouts, suggesting that broccoli sprouts can serve as a suitable source for sulforaphane in intervention trials. A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Time: length of treatment Compound Based Treatment: LNCaP cells were treated with 10 or 25 uM L-sulforaphane, broccoli extract or DMSO Keywords: compound_treatment_design Computed
2009-01-20 | E-GEOD-14364 | biostudies-arrayexpress
Project description:Consumption of a diet rich in cruciferous vegetables is associated with decreased risk of developing non-communicable chronic disease. It has been proposed that biologically active isothiocyanates (ITCs) obtained from these vegetables, such as sulforaphane (SF) derived from broccoli, are responsible for mediating health benefits via multiple mechanisms of action. ITCs have been shown to suppress the levels of several LPS-induced pro-inflammatory cytokines that are biomarkers for chronic inflammatory conditions, and which have been associated with the development of both cancer and cardiovascular disease. In patients suffering from chronic inflammatory diseases, LPS is elevated in circulation to levels reaching around 1ng/ml. In the current study, we demonstrate that SF suppresses global changes in gene expression induced by LPS exposure (1ng/ml) in human THP-1 cells at a physiologically achievable concentration of 5 micromolar. These results illustrate the profound effect that SF can have at concentrations achievable through the consumption of broccoli in suppressing TLR4-mediated inflammatory pathways.
2014-12-03 | E-MEXP-3931 | biostudies-arrayexpress
Project description:Difference between sulforaphane and sulforaphene in colon cancer
| PRJNA729976 | ENA
Project description:BACKGROUND. Prostate cancer is thought to arise as a result of oxidative stresses and induction of antioxidant electrophile defense (phase 2) enzymes has been proposed as a prostate cancer prevention strategy. The isothiocyanate sulforaphane, derived from cruciferous vegetables like broccoli, potently induces surrogate markers of phase 2 enzyme activity in prostate cells in vitro and in vivo. To better understand the temporal effects of sulforaphane and broccoli sprouts on gene expression in prostate cells, we carried out comprehensive transcriptome analysis using cDNA microarrays. METHODS. Transcripts significantly modulated by sulforaphane over time were identified using StepMiner analysis. Ingenuity Pathway Analysis (IPA) was used to identify biological pathways, networks, and functions significantly altered by sulforaphane treatment. . StepMiner and IPA revealed significant changes in many transcripts associated with cell growth and cell cycle, as well as a significant number associated with cellular response to oxidative damage and stress. Comparison to an existing dataset suggested that sulforaphane blocked cell growth by inducing G2/M arrest. Cell growth assays and flow cytometry analysis confirmed that sulforaphane inhibited cell growth and induced cell cycle arrest. CONCLUSIONS. Our data suggest that in prostate cells sulforaphane primarily induces cellular defenses and inhibits cell growth by causingG2/Mphase arrest. Furthermore, based on the striking similarities in the gene expression patterns induced across experiments in these cells, sulforaphane appears to be the primary bioactive compound present in broccoli sprouts, suggesting that broccoli sprouts can serve as a suitable source for sulforaphane in intervention trials. A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Time: length of treatment Compound Based Treatment: LNCaP cells were treated with 10 or 25 uM L-sulforaphane, broccoli extract or DMSO Keywords: compound_treatment_design
2009-01-21 | GSE14364 | GEO
Project description:Epidemiological studies provide strong evidence that consumption of cruciferous vegetables, such as broccoli, can significantly reduce the risk of developing cancers. Sulforaphane (SFN), a phytochemical derived from cruciferous vegetables, induces anti-proliferative and pro-apoptotic responses in prostate cancer cells, but not in normal prostate cells. The mechanisms responsible for these specific chemopreventive properties remain unclear. We utilized RNA sequencing to test the hypothesis that SFN modifies the expression of genes that are critical in prostate cancer progression. Normal prostate epithelial cells, and androgen-dependent and androgen-independent prostate cancer cells were treated with 15 µM SFN and the transcriptome was determined at 6 and 24 hour time points. SFN altered the expression of ~3,000 genes in each cell line and the response was highly dynamic over time. SFN influenced the expression of genes in functional groups and pathways that are critical in cancer including cell cycle, apoptosis and angiogenesis, but the specific effects of SFN differed depending on the state of cancer progression. Network analysis suggested that a transcription factor that is overexpressed in many cancers, Specificity protein 1 (Sp1), is a major mediator of SFN-induced changes in gene expression. Nuclear Sp1 protein was significantly decreased by 24 hour SFN treatment in prostate cancer cells, while a related transcription factor, Sp3 protein was only modestly decreased in androgen-independent prostate cancer cells. Overall, the data show that SFN significantly affects gene expression in normal and cancer cells, with key targets in chemopreventive processes, making it a promising dietary anti-cancer agent.
2014-07-11 | GSE48812 | GEO
Project description:Sulforaphane (SFN) is an isothiocyanate present in cruciferous vegetables that ameliorates various disease models in rodents (e.g., cancer, diabetes, seizures) that are likewise mitigated by dietary restriction leading us to test the hypothesis that this compound elicits cellular responses consistent with being a fasting mimetic. Using untransformed human retinal pigment epithelial (RPE-1) cells, we report that SFN impacted multiple nutrient-sensing pathways consistent with a fasting state. SFN treatment (i) increased mitochondrial resistance to oxidative stress, (ii) acutely suppressed markers of mTORC1/2 activity via inhibition of insulin signaling, (iii) upregulated autophagy and further amplified autophagic flux induced by rapamycin or nutrient deprivation while concomitantly promoting lysosomal and mitochondrial biogenesis, (iv) acutely decreased glucose uptake and lactate secretion followed by an adaptive rebound that coincided with suppressed protein levels of thioredoxin-interacting protein (TXNIP) due to early transcriptional down-regulation. This early suppression of TXNIP mRNA expression could be overcome with exogenous glucosamine consistent with SFN inhibiting glutamine F6P amidotransferase (GFAT), the rate limiting enzyme of the hexosamine biosynthetic pathway. SFN also altered multiple glycolytic and tricarboxylic acid (TCA) cycle intermediates while reducing the inhibitory phosphorylation on pyruvate dehydrogenase, indicative of an adaptive cellular starvation response directing pyruvate into acetyl coenzyme A for uptake by the TCA cycle. RNA-seq of cells treated for 4hrs with SFN confirmed the activation of signature starvation-responsive transcriptional programs. Concomitant with stabilizing and activating the transcription factor NF-E2-related factor 2, we posit that the fasting-mimetic properties of SFN underlie both the therapeutic efficacy and potential toxicity of this phytochemical.
2024-11-28 | GSE275316 | GEO
Project description:Sulforaphane (SFN), an isothiocyanate found in cruciferous vegetables, is a potent inhibitor of experimental mammary carcinogenesis and may be an effective, safe chemopreventive agent for use in humans. SFN acts in part on the Keap1/Nrf2 pathway to regulate a battery of cytoprotective genes. In this study transcriptomic and proteomic changes in the estrogen receptor negative, non tumorigenic human breast epithelial MCF10A cell line were analyzed following SFN treatment or KEAP1 knockdown with siRNA using microarray and stable isotopic labeling with amino acids in culture (SILAC), respectively. Changes in selected transcripts and proteins were confirmed by PCR and Western blot in MCF10A and MCF12A cells. There was strong correlation between the transcriptomic and proteomic responses in both the SFN treatment (R=0.679, P<0.05) and KEAP1 knockdown (R=0.853, P<0.05) experiments. Common pathways for SFN treatment and KEAP1 knockdown were xenobiotic metabolism and antioxidants, glutathione metabolism, carbohydrate metabolism and NADH/NADPH regeneration. Moreover, these pathways were most prominent in both the transcriptomic and proteomic analyses. The aldo-keto reductase family members, AKR1B10, AKR1C1, AKR1C2 and AKR1C3, as well as NQO1 and ALDH3A1, were highly upregulated at both the transcriptomic and proteomic level. Collectively, these studies served to identify potential biomarkers that can be used in clinical trials to investigate the initial pharmacodynamic action of SFN in the breast. MCF10A cells were treated with SFN or had KEAP1 knocked down by siRNA.
2011-04-22 | E-GEOD-28813 | biostudies-arrayexpress
Project description:Sulforaphane (SFN), an isothiocyanate found in cruciferous vegetables, is a potent inhibitor of experimental mammary carcinogenesis and may be an effective, safe chemopreventive agent for use in humans. SFN acts in part on the Keap1/Nrf2 pathway to regulate a battery of cytoprotective genes. In this study transcriptomic and proteomic changes in the estrogen receptor negative, non tumorigenic human breast epithelial MCF10A cell line were analyzed following SFN treatment or KEAP1 knockdown with siRNA using microarray and stable isotopic labeling with amino acids in culture (SILAC), respectively. Changes in selected transcripts and proteins were confirmed by PCR and Western blot in MCF10A and MCF12A cells. There was strong correlation between the transcriptomic and proteomic responses in both the SFN treatment (R=0.679, P<0.05) and KEAP1 knockdown (R=0.853, P<0.05) experiments. Common pathways for SFN treatment and KEAP1 knockdown were xenobiotic metabolism and antioxidants, glutathione metabolism, carbohydrate metabolism and NADH/NADPH regeneration. Moreover, these pathways were most prominent in both the transcriptomic and proteomic analyses. The aldo-keto reductase family members, AKR1B10, AKR1C1, AKR1C2 and AKR1C3, as well as NQO1 and ALDH3A1, were highly upregulated at both the transcriptomic and proteomic level. Collectively, these studies served to identify potential biomarkers that can be used in clinical trials to investigate the initial pharmacodynamic action of SFN in the breast.
2011-04-22 | GSE28813 | GEO
Project description:FSH is considered as the most critical regulatory factor for follicle growth and development. It is widely acknowledged that exogenous administration of FSH can effectively stimulate ovulation.However, these techniques have several drawbacks such as high cost and detrimental effects on hormone balance and embryo implantation.Sulforaphane (SFN) is a naturally occurring compound that belongs to the isothiocyanate group, which is predominant in cruciferous vegetables.Our previous research demonstrated SFN could inhibit hypoxia-evoked apoptosis in porcine GCs. Intriguingly, SFN exhibits a biphasic dose-response, stimulating cell growth at low doses in various mammalian cells. Therefore,to investigate the functional implications of sulforaphane in the regulation of granulosa cell proliferation, we conducted a gene expression profiling analysis using RNA-seq data, comparing SFN to follicle stimulating hormone (FSH).
2024-10-01 | GSE233365 | GEO