Selected isothiocyanates rapidly induce growth inhibition of cancer cells.

Paper

Selected isothiocyanates rapidly induce growth inhibition of cancer cells.

Published Oct 1, 2003 · Yuesheng Zhang, L. Tang, V. Gonzalez

Molecular cancer therapeutics

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226

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6

Influential Citations

Semantic Scholar

Abstract

Many plant-derived isothiocyanates (ITCs), which occur in human diet, are potent cancer chemopreventive agents in animals. Among the anticarcinogenic mechanisms that have been revealed for ITCs is the inhibition of cell proliferation. We report that exposure of cancer cells to either allyl-ITC (AITC), benzyl-ITC (BITC), or phenethyl-ITC (PEITC) for only 3 h was long enough for the inhibition of cell growth, based on a comparison of IC50 values; regardless of the origin of cancer cells; and even in drug-resistant cells that overexpressed multidrug resistance associated protein-1 (MRP-1) or P-glycoprotein-1 (Pgp-1). In contrast, the inhibitory effect of another ITC, sulforaphane (SF), on these cells was highly time dependent. The finding that some ITCs could inhibit the proliferation of cancer cells in a largely time-independent manner is significant because ITCs that enter the human body are rapidly cleared through urinary excretion. Using human promyelocytic leukemia HL60/S as model cells, and focusing on AITC and BITC, we found that these ITCs modulated multiple cellular targets involved in proliferation, including the disruption of mitochondrial membrane potential, activation of multiple caspases, arrest of cell cycle progression, and induction of differentiation. Again, only a 3-h incubation of the cells with the ITCs was enough to exert their full effect on these targets. Taken together, our findings suggest that selected ITCs can rapidly initiate growth inhibition of cancer cells by simultaneously modulating multiple cellular targets, and their antiproliferative activity may be largely unaffected by their metabolism and disposition in vivo.

In Vitro Study

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Select isothiocyanates rapidly inhibit cancer cell growth by modulating multiple cellular targets, with their antiproliferative activity potentially unaffected by metabolism and disposition in vivo.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Selected isothiocyanates rapidly induce growth inhibition of cancer cells.

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References

Isothiocyanates as cancer chemopreventive agents: their biological activities and metabolism in rodents and humans.

Isothiocyanates, found in cruciferous vegetables, show potential as cancer chemopreventive agents by inhibiting tumor development in experimental models and through their metabolism in rodents and humans.

High cellular accumulation of sulphoraphane, a dietary anticarcinogen, is followed by rapid transporter-mediated export as a glutathione conjugate.

Sulphoraphane's anticarcinogenic activity depends on its accumulation levels in cells, but its rapid export as a glutathione conjugate limits its potential for effective dosing regimens.

Growth inhibition, cell-cycle arrest and apoptosis in human T-cell leukemia by the isothiocyanate sulforaphane.

Sulforaphane, a synthetic isothiocyanate, can inhibit leukemic cell growth and induce apoptosis, making it a potential chemopreventive/chemotherapeutic agent.

Sulforaphane and its metabolite mediate growth arrest and apoptosis in human prostate cancer cells.

Sulforaphane and its metabolite SFN-NAC, found in broccoli and other cruciferous vegetables, mediate growth arrest and apoptosis in prostate cancer cells, potentially aiding in prostate cancer prevention.

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A sensitive and specific method has been developed for quantifying dithiocarbamate levels in human plasma, serum, and erythrocytes, important for determining dosing regimens for dietary isothiocyanates and their metabolites.

Decomposition rates of isothiocyanate conjugates determine their activity as inhibitors of cytochrome p450 enzymes.

Thiol-ITCs' tumor inhibitory activity may not solely be due to inhibition of carcinogen activation by parent isothiocyanates released from thiol-ITCs, but may involve other mechanisms.

Induction of histone acetylation in mouse erythroleukemia cells by some organosulfur compounds including allyl isothiocyanate

Allyl isothiocyanate can cause increased acetylation of histones in mouse erythroleukemia cells, but the mechanism for this effect requires further elucidation.

Chemoprotective glucosinolates and isothiocyanates of broccoli sprouts: metabolism and excretion in humans.

Broccoli sprouts' chemoprotective glucosinolates and isothiocyanates are more bioavailable than their glucosinolates, with thorough chewing increasing dithiocarbamate excretion.

Dietary intake of isothiocyanates: evidence of a joint effect with glutathione S-transferase polymorphisms in lung cancer risk.

Low dietary intake of isothiocyanates and the GSTT1 null genotype are associated with increased lung cancer risk in current smokers.

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