Sulforaphane and its glutathione conjugate but not sulforaphane nitrile induce UDP-glucuronosyl transferase (UGT1A1) and glutathione transferase (GSTA1) in cultured cells

Basten, Graham; Bao, Yongping; Williamson, Gary

doi:10.1093/carcin/23.8.1399

Cited by 133 publications

(90 citation statements)

References 45 publications

(45 reference statements)

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“…Therefore it is coming up as an economical, easily available, and novel approach to cancer treatment and management (Karikas, 2010). Sulforaphane is an isothiocyanate, found in cruciferous vegetables, such as broccoli, kale, and cauliflower displays significant chemopreventive activity resulting from its inhibition of carcinogen-activating enzymes and induction of detoxification enzymes affecting carcinogen metabolism and disposition and by modulating epigenetic machinery (Barcelo et al, 1996;Basten et al, 2002;Myzak et al, 2006;Gibbs et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

Sulforaphane Inhibits Growth of Human Breast Cancer Cells and Augments the Therapeutic Index of the Chemotherapeutic Drug, Gemcitabine

Hussain¹,

Mohsin²,

Prabhu³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Phytochemicals are among the natural chemopreventive agents with most potential for delaying, blocking or reversing the initiation and promotional events of carcinogenesis. They therefore offer cancer treatment strategies to reduce cancer related death. One such promising chemopreventive agent which has attracted considerable attention is sulforaphane (SFN), which exhibits anti-cancer, anti-diabetic, and anti-microbial properties. The present study was undertaken to assess effect of SFN alone and in combination with a chemotherapeutic agent, gemcitabine, on the proliferative potential of MCF-7 cells by cell viability assay and authenticated the results by nuclear morphological examination.

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Section: Discussionmentioning

confidence: 99%

Sulforaphane Inhibits Growth of Human Breast Cancer Cells and Augments the Therapeutic Index of the Chemotherapeutic Drug, Gemcitabine

Hussain¹,

Mohsin²,

Prabhu³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…In human HepG2 cells, for example, SFN increases mRNA of UDP-glucuronosyltranferase (UGT) 1A1 and GSTA1 [7], increases QR activity [11], and increases UGT1A1 protein as well as bilirubin glucuronidation [12]. An increase in GST and QR activities also was observed with SFN treatment in murine Hepa1c1c7 cells [11,13].…”

Section: Modulation Of Phase 2 Enzymesmentioning

confidence: 94%

Chemoprotection by sulforaphane: Keep one eye beyond Keap1

2006

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Sulforaphane (SFN) is an isothiocyanate found in cruciferous vegetables, with particularly high levels detected in broccoli and broccoli sprouts. Over a decade ago, this phytochemical was identified as a likely chemopreventive agent based on its ability to induce Phase 2 detoxification enzymes, as well as to inhibit Phase 1 enzymes involved in carcinogen activation. Considerable attention has focused on SFN as a 'blocking' agent, with the ability to modulate the Nrf2/Keap1 pathway, but recent evidence suggests that SFN acts by numerous other mechanisms. SFN induces cell cycle arrest and apoptosis in cancer cells, inhibits tubulin polymerization, activates checkpoint 2 kinase, and inhibits histone deacetylase activity. The latter findings suggest that SFN may be effective during the postinitiation stages of carcinogenesis, as a 'suppressing' agent. Moreover, pharmacological administration of SFN may be a promising therapeutic approach to the treatment of cancers, including those characterized by increased inflammation and involving viral or bacterial-related pathologies. The present review discusses the more widely established chemoprotective mechanisms of SFN, but makes the case for additional work on mechanisms that might be of importance during later stages of carcinogenesis, beyond Keap1.

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“…Primer pairs specific for human UGT1A1 (5Ј-GGT GAC TGT CCA GGA CCT ATT GA-3Ј and 5Ј-TAG TGG ATT TTG GTG AAG GCA GTT-3Ј) and biliverdin reductase (5Ј-GGA AGA GAC CAA GAT GAA TA-3Ј and 5Ј-CAA GAG TTC AAC ATG CTC-3Ј) were utilized for amplification, 39,40 with the rig/S15 small ribosomal subunit protein (5Ј-TTC CGC AAG TTC ACC TAC C-3Ј and 5Ј-CGG GCC GGC CAT GCT TTA CG-3Ј) serving as control. Reactions were subjected to 35 cycles at 95°C for 1 min, 58°C for 1 min and 72°C for 2 min.…”

Section: Semiquantitative Rt-pcr Analysismentioning

confidence: 99%

Unconjugated bilirubin induces apoptosis in colon cancer cells by triggering mitochondrial depolarization

Keshavan¹,

Schwemberger²,

Smith³

et al. 2004

Intl Journal of Cancer

112

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Bilirubin is the principal end product of heme degradation. Prompted by epidemiologic analyses demonstrating an inverse correlation between serum bilirubin levels and cancer mortality, we examined the effect(s) of bilirubin on the growth and survival of colon adenocarcinoma cells. Adenocarcinoma cell monolayers were treated with bilirubin over a range of bilirubin:BSA molar ratios (0 -0.6), and viability was assessed colorimetrically. Apoptosis was characterized by TUNEL assay, annexin V staining and caspase-3 activation. The mechanism(s) by which bilirubin induces apoptosis was investigated by Western blotting for cytochrome c release, assaying for caspase-8 and caspase-9 activation and for mitochondrial depolarization by JC-1 staining. The direct effect of bilirubin on the membrane potential of isolated mitochondria was evaluated using light-scattering and fluorescence techniques. Bilirubin decreased the viability of all colon cancer cell lines tested in a dose-dependent manner. Cells exhibited substantial apoptosis when exposed to bilirubin concentrations ranging 0 -50 M, as demonstrated by an 8-to 10-fold increase in TUNEL and annexin V staining and in caspase-3 activity. Bilirubin treatment evokes specific activation of caspase-9, enhances cytochrome c release into the cytoplasm and triggers the mitochondrial permeability transition in colon cancer monolayers. Additionally, bilirubin directly induces the depolarization of isolated rat liver mitochondria, an effect that is not inhibited by cyclosporin A. Bilirubin stimulates apoptosis of colon adenocarcinoma cells in vitro through activation of the mitochondrial pathway, apparently by directly dissipating mitochondrial membrane potential. As this effect is triggered at concentrations normally present in the intestinal lumen, we postulate a physiologic role for bilirubin in modulating colon tumorigenesis.

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Sulforaphane and its glutathione conjugate but not sulforaphane nitrile induce UDP-glucuronosyl transferase (UGT1A1) and glutathione transferase (GSTA1) in cultured cells

Cited by 133 publications

References 45 publications

Sulforaphane Inhibits Growth of Human Breast Cancer Cells and Augments the Therapeutic Index of the Chemotherapeutic Drug, Gemcitabine

Sulforaphane Inhibits Growth of Human Breast Cancer Cells and Augments the Therapeutic Index of the Chemotherapeutic Drug, Gemcitabine

Chemoprotection by sulforaphane: Keep one eye beyond Keap1

Unconjugated bilirubin induces apoptosis in colon cancer cells by triggering mitochondrial depolarization

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