Antimetastatic activity of Sulforaphane

Thejass, P.; Kuttan, Girija

doi:10.1016/j.lfs.2005.12.038

Cited by 85 publications

(59 citation statements)

References 33 publications

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“…5 M (PEITC) [93] 10 M (PEITC) [94] 5 M (SFN) [90] 15 M (SFN) [91] 5 M (BITC) [43] 10 M (PEITC) [95] Induction of Appears to require higher concentrations 25 M (PEITC/BITC) A c c e p t e d M a n u s c r i p t necrosis than induction of apoptosis [96] 50 m (BITC) [97] Metastasis ITCs inhibit cell adhesion, invasion and migration in vitro, and metastasis in vivo 5 M (AITC) [98] 5 M (PEITC) [99] 2 M (PEITC) [24] 2 g/ml (SFN) [100] Inhibition of angiogenesis ITCs inhibit angiogenesis in in vitro and in vivo models 1 M (PEITC) [24] 5 g/ml (AITC) [27] 0.1 -1 M (SFN) [23] Page 30 of 38…”

Section: Discussionmentioning

confidence: 99%

Anti-angiogenic effects of dietary isothiocyanates: Mechanisms of action and implications for human health

Cavell

Alwi

Donlevy

et al. 2011

Biochemical Pharmacology

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To cite this version:Breeze E. Cavell, Sharifah S. Syed Alwi, Alison Donlevy, Graham Packham. Anti-angiogenic effects of dietary isothiocyanates; mechanisms of action and implications for human health. Biochemical Pharmacology, Elsevier, 2010, 81 (3) This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 Isothiocyanates and angiogenesis -3 - AbstractIsothiocyanates (ITCs) are electrophilic compounds derived from plants and are thought to play a major role in the potential chemopreventive effects associated with high intake of cruciferous vegetables. ITCs are also being evaluated for chemotherapeutic activity in early phase clinical trials. In addition to their effects on carcinogen metabolism and cancer cell survival and proliferation, ITCs have been shown to effectively interfere with angiogenesis in vitro and in vivo. Angiogenesis is the development of a new blood supply from existing vasculature and is required for tumours to develop beyond a small size limit determined by the diffusion limit for oxygen. Inhibition of angiogenesis may play a key role in the potential chemopreventive/chemotherapeutic activity of ITCs. In this review we highlight recent data demonstrating that ITCs have anti-angiogenic activity and identify potential molecular targets for these effects, including hypoxia-inducible factor (HIF), nuclear factor B (NF-B), activator protein 1 (AP1) and tubulin. We also discuss these findings in light of the potential chemopreventive/chemotherapeutic effects of ITCs.

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Section: Discussionmentioning

confidence: 99%

Anti-angiogenic effects of dietary isothiocyanates: Mechanisms of action and implications for human health

Cavell

Alwi

Donlevy

et al. 2011

Biochemical Pharmacology

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“…The Cdk1/ cyclin B1 complex is retained in an inactive state by reversible phosphorylation at Thr 14 and Tyr 15 of Cdk1 (31,32). Dephosphorylation of Cdk1, and hence activation of Cdk1/cyclin B1 kinase complex, is catalyzed by Cdc25B and Cdc25C, and this reaction is believed to be a ratelimiting step for entry into mitosis (33).…”

Section: Effect Of Sfn Treatment On Levels Of G 1 -S and G 2 -M Specimentioning

confidence: 99%

“…Cancer chemoprevention by L-SFN or SFN has been observed against 9,10-dimethyl-1,2-benzanthraceneinduced mammary cancer in rats, azoxymethane-induced colonic aberrant crypt foci in rats, benzo [a]pyrene-induced forestomach cancer in mice, and 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol 13-acetate -induced skin tumorigenesis in mice (8, 11 -13). More recently, SFN administration was shown to significantly inhibit lung metastasis induced by B16F-10 melanoma cells in C57BL/6 mice (14).…”

Section: Introductionmentioning

confidence: 98%

Induction of p21 protein protects against sulforaphane-induced mitotic arrest in LNCaP human prostate cancer cell line

Herman-Antosiewicz

Xiao

Lew

et al. 2007

Molecular Cancer Therapeutics

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Previous studies have indicated that D,L-sulforaphane (SFN), a synthetic cancer chemopreventive analogue of cruciferous vegetable-derived isomer (À)-1-isothiocyanato-(4R)-(methylsulfinyl)-butane, activates a checkpoint kinase 2 (Chk2) -dependent G 2 -M phase cell cycle arrest in p53-deficient human prostate cancer cells. Because p53 is a downstream target of Chk2 kinase and known to regulate G 2 -M transition by transcriptional regulation of cyclin-dependent kinase (Cdk) inhibitor p21Cip1/Waf1 (p21), the present study was undertaken to determine the role of p21 in SFN-induced cell cycle arrest using wild-type p53 -expressing cell line LNCaP. The SFN treatment caused a modest increase in S phase fraction and a marked increase in G 2 -M fraction in LNCaP cells in a concentration-and time-dependent manner. The SFN-induced S phase arrest correlated with a reduction in protein levels of cyclin D1, cyclin E, Cdk4, and Cdk6, whereas activation of the G 2 -M checkpoint was accompanied by induction of cyclin B1 and down-regulation of Cdk1 and Cdc25C protein levels. The SFN-treated LNCaP cells were also arrested in mitosis as revealed by immunofluorescence microscopy and increased Ser 10 phosphorylation of histone H3, a sensitive marker for mitotic cells. The SFN treatment increased activating phosphorylation of Chk2 (Thr 68 ) that was accompanied by induction of p53 and p21. The SFNinduced mitotic arrest was statistically significantly increased by small interfering RNA -based knockdown of p21. However, p21 protein knockdown did not have any appreciable effect on SFN-induced cytoplasmic histoneassociated DNA fragmentation (apoptosis). In conclusion, the present study indicates that induction of p21 protects against SFN-induced mitotic arrest in LNCaP cells. [Mol Cancer Ther 2007;6(5):1673 -81]

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“…Others have indicated that sulforaphane acts as a potential HDAC inhibitor and an inducer of various pro-apoptotic molecules (12)(13)(14). Sulforaphane was also found to inhibit prostate tumor growth and lung metastasis in a melanoma model (15,16).Matrix metalloproteinases (MMPs) are extracellular matrix proteins known to play a crucial role in normal physiological processes, such as embryogenesis, wound healing, morphogenesis, reproduction, tissue resorption and remodeling, and in pathological processes, such as inflammation, arthritis, cancer, cardiovascular and pulmonary diseases; hence, they are considered therapeutic targets (17,18). Certain mmps act as tumor suppressors, whereas others act as tumor promoters.…”

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confidence: 99%

Quercetin and sulforaphane in combination suppress the progression of melanoma through the down-regulation of matrix metalloproteinase-9

Pradhan

Mishra

Sharma

et al. 2010

Experimental and Therapeutic Medicine

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Abstract. malignant melanoma is one of the most common types of cancer in the uS and worldwide. the epidemiological data suggest that dietary modification may reduce the incidence of this disease. Quercetin (3,5,7,3',4'-tetrahydroxyflavone), a flavonoid isolated from onion, exhibits anti-oxidant, anti-inflammatory and anti-cancer effects. D,L-sulforaphane [1-isothiocyanato-4-(methylsulfinyl)-butane], a cruciferous vegetable-derived isomer isolated from broccoli, is highly effective in protection against cancer. Matrix metalloproteinases (MMPs), extracellular matrix degrading enzymes, are involved in embryogenesis, inflammation, angiogenesis and cancer. mmp-9 in particular plays a crucial role in the regulation of invasion, tumor growth and metastasis. Previous studies have reported that both quercetin and sulforaphane independently reduce tumor growth and metastasis in breast, prostate, lung and other types of cancers. However, the combined effects of quercetin and sulforaphane on the regulation of tumor growth and the mechanism(s) of actions underlying this process have not yet been investigated. In the present study, we report for the first time that quercetin and sulforaphane in combination inhibit the proliferation and migration of melanoma (B16F10) cells more effectively than either compound used alone. Moreover, these compounds in combination significantly suppressed melanoma growth as compared to their individual use in a mouse model. This combined effect was predominantly due to a decrease in mmp-9 expression in the mouse tumors. taken together, our findings revealed that the administration of quercetin and sulforaphane in combination rather than alone may be a more effective approach for the treatment of malignant melanoma. Introductionmalignant melanoma is one of the most common types of cancer in the US as well as worldwide. It is an aggressive disease with high metastatic potential and resistance to many cytotoxic agents (1). Melanoma cells have low levels of spontaneous apoptosis, and chemotherapeutic drugs function by inducing apoptosis (1). Many dietary agents, including kinase inhibitors, have been inversely correlated to the spread of malignant melanoma (2-4). The alkylating agent dacarbazine is currently being used in clinical trials in combination with novel therapeutic agents (4). Quercetin (3,5,7,3' ,4'-tetrahydroxyflavone) is a flavonoid isolated from onion, whereas sulforaphane [1-isothiocyanato-4-(methylsulfinyl)-butane] is a member of an isothiocyanate family of chemopreventive agents isolated from broccoli. The anti-cancer properties of these compounds have been demonstrated in a number of malignancies, including prostate, breast, skin and liver cancers (5-9). Previous reports suggest that quercetin is an anti-oxidant and anti-inflammatory compound (10,11). Others have indicated that sulforaphane acts as a potential HDAC inhibitor and an inducer of various pro-apoptotic molecules (12)(13)(14). Sulforaphane was also found to inhibit prostate tumor growth and lung metastasis in a melanoma...

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Antimetastatic activity of Sulforaphane

Cited by 85 publications

References 33 publications

Anti-angiogenic effects of dietary isothiocyanates: Mechanisms of action and implications for human health

Anti-angiogenic effects of dietary isothiocyanates: Mechanisms of action and implications for human health

Induction of p21 protein protects against sulforaphane-induced mitotic arrest in LNCaP human prostate cancer cell line

Quercetin and sulforaphane in combination suppress the progression of melanoma through the down-regulation of matrix metalloproteinase-9

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