Sulforaphane-mediated induction of a phase 2 detoxifying enzyme NAD(P)H:quinone reductase and apoptosis in human lymphoblastoid cells.

Misiewicz, Irena; Skupińska, Katarzyna; Kowalska, E; Lubiński, Jan; Kasprzycka‐Guttman, T.

doi:10.18388/abp.2004_3556

Cited by 47 publications

(16 citation statements)

References 28 publications

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“…In our cytotoxicity results, the values of CC 50 for these paired cells are 12/33 µM and 15/11 µM, respectively (Figure ). In other reports, it was suggested that the IC 50 values of SFN were 1–10 µM in colon cancer cell lines , 18 and 20 µM in human leukemia cells , 3.9 µM in human lymphoblastoid cells and 8.1–9.5 µM in human breast cancer cells . Therefore, SFN showed similar cytotoxicity in NPC cells to other types of cancer cells.…”

Section: Discussionmentioning

confidence: 76%

Inhibition of epstein‐barr virus reactivation in nasopharyngeal carcinoma cells by dietary sulforaphane

Chuang

Lin

et al. 2012

Molecular Carcinogenesis

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Epstein-Barr virus (EBV) has been associated with several human malignancies including nasopharyngeal carcinoma (NPC). Reactivation of latent EBV has been considered to contribute to the carcinogenesis of NPC. Blocking the EBV lytic cycle has been shown effective in the treatment of EBV-associated diseases. We have searched for natural dietary compounds inhibiting EBV reactivation in NPC cells. Among them, sulforaphane (SFN) was found to be effective in the inhibition of EBV reactivation in latent EBV-positive NPC cells, NA and HA. SFN is a histone deacetylase (HDAC) inhibitor and has been recognized as an antioxidant and antitumor compound for chemoprevention. However, its antiviral effect is less well elucidated. In this study, after determination of the cytotoxicity of SFN on various epithelial cells, we showed that SFN treatment inhibits EBV reactivation, rather than induction, by detection of EBV lytic gene expression in EBV-positive NPC cells. We also determined that the number of cells supporting the EBV lytic cycle is decreased using immunofluorescence and flow cytometric analysis. Moreover, we have found that this inhibitory effect decreases virus production. To elucidate the inhibitory mechanism of SFN on the EBV lytic cycle, luciferase reporter assays were carried out on the Zta and Rta promoters. The results show that SFN inhibits transactivation activity of the EBV immediate-early gene Rta but not Zta. Together, our results suggest that SFN has the capability to inhibit EBV lytic cycle and the potential to be taken as a dietary compound for prevention of EBV reactivation.

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Section: Discussionmentioning

confidence: 76%

Inhibition of epstein‐barr virus reactivation in nasopharyngeal carcinoma cells by dietary sulforaphane

Chuang

Lin

et al. 2012

Molecular Carcinogenesis

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“…SFN has been well known as a potent inducer of the phase II antioxidant enzymes including HO‐1 [2,3]. Treatment of mouse cortical cells with SFN resulted in a significant induction of HO‐1 together with an increase in ARE reporter activity (Supplemental Fig.…”

Section: Discussionmentioning

confidence: 97%

Sulforaphane induces autophagy through ERK activation in neuronal cells

Kim

Cho

et al. 2014

FEBS Letters

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a b s t r a c t Sulforaphane (SFN), an activator of nuclear factor E2-related factor 2 (Nrf2), has been reported to induce autophagy in several cells. However, little is known about its signaling mechanism of autophagic induction. Here, we provide evidence that SFN induces autophagy with increased levels of LC3-II through extracellular signal-regulated kinase (ERK) activation in neuronal cells. Pretreatment with NAC (N-acetyl-L-cysteine), a well-known antioxidant, completely blocked the SFN-induced increase in LC3-II levels and activation of ERK. Knockdown or overexpression of Nrf2 did not affect autophagy. Together, the results suggest that SFN-mediated generation of reactive oxygen species (ROS) induces autophagy via ERK activation, independent of Nrf2 activity in neuronal cells.

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“…A representative compound of new generation PP(Ala) 2 (Arg) 2 -dialanine derivative of protoporphyrin IX was investigated as a potentially more effective drug in comparison to the PPIX to PDT (Graczyk & Konarski, 1995, Graczyk & Konarski, 1997Graczyk, 1999). The cell viability under influence of PDT depending on time after irradiation (controls: non-toxic energy doses and photosensitizer concentrations) and then cell death mechanism by transmembrane mitochondrial potential -early stage of apoptosis were studied (Misiewicz et al, 2003;Misiewicz et al, 2004;Misiewicz-Krzemińska et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

“…In healthy cells (polarized mitochondria) the dye accumulates and forms J-aggregates giving red fluorescence. In apoptotic cells (depolarized mitochondria) monomeric dye gives green fluorescence (the dye stays in the cytoplasm) (Misiewicz et al, 2003;Misiewicz et al, 2004;Misiewicz-Krzemińska et al, 2009;Reers et al, 1991;Smiley et al, 1991).…”

Section: Chemicalsmentioning

confidence: 99%

Cytotoxicity of PP(Arg)2- and PP(Ala)2(Arg)2-based photodynamic therapy and early stage of apoptosis induction in human breast cancers in vitro.

Nowak-Stępniowska¹,

Wiktorska²,

Małecki³

et al. 2012

Acta Biochim Pol

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Mitochondria are cell energetic centers where ATP is produced. They also play a very important role in the PDT as intracellular sites of photosensitizer localization. Photosensitizers gathering in mitochondria (like porphyrin derivatives used in this work) are more effective in tumor cell destruction. Moreover, it was assumed that di-amino acid substituents attached to porphyrin ring will strengthen the effectivity of interaction with membrane receptors of examined cells. MTT assay was performed to investigate the influence of PP(Arg) 2 and PP(Ala) 2 (Arg) 2 -based PDT on breast cancer cell viability for 24 h, 48 h and 120 h after cell irradiation. Then the influence of PP(Ala) 2 (Arg) 2 -and PP(Arg) 2 -mediated PDT on early mitochondrial apoptosis induction via measurements of the transmembrane mitochondrial potential changes was examined. Results showed that lower energy doses and maximal nontoxic photosensitizer doses of PP(Ala) 2 (Arg) 2 and PP(Arg) 2 applied in PDT can imply apoptotic cell death. It was confirmed that modification of the protoporphyrin IX by attaching two alanine substituents raised the efficiency of photodynamic therapy.

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Sulforaphane-mediated induction of a phase 2 detoxifying enzyme NAD(P)H:quinone reductase and apoptosis in human lymphoblastoid cells.

Cited by 47 publications

References 28 publications

Inhibition of epstein‐barr virus reactivation in nasopharyngeal carcinoma cells by dietary sulforaphane

Inhibition of epstein‐barr virus reactivation in nasopharyngeal carcinoma cells by dietary sulforaphane

Sulforaphane induces autophagy through ERK activation in neuronal cells

Cytotoxicity of PP(Arg)2- and PP(Ala)2(Arg)2-based photodynamic therapy and early stage of apoptosis induction in human breast cancers in vitro.

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