Anti-carcinogenic effects of sulforaphane in association with its apoptosis-inducing and anti-inflammatory properties in human cervical cancer cells

Sharma, Chhavi; Sadrieh, Lida; Priyani, Anita; Ahmed, Musthaq; Hassan, Ahmad; Hussain, Arif

doi:10.1016/j.canep.2010.09.008

Cited by 53 publications

(44 citation statements)

References 58 publications

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“…This implies that there are yet other factors that contribute to cell death initiated by these compounds. Several reports have shown that both WA and SFN are effective in the inhibition of pro-inflammatory cytokines, as well as the aberrant expression of epigenetic modifiers [11,13,[33][34][35]. Moreover, Hahm and colleagues reported that WA-induced apoptosis was mediated through reactive oxygen species and Nagalingam et al found that WA inhibited breast tumor formation in vivo through the activation of the ERK/RSK axis, DR5 upregulation, and elevated nuclear accumulation of Elk1 and CHOP in breast cancer [19,36].…”

Section: Discussionmentioning

confidence: 99%

Novel Combination of Withaferin A and Sulforaphane Inhibits Epigenetic Machinery, Cellular Viability and Induces Apoptosis of Breast Cancer Cells

Royston¹,

Udayakumar²,

Lewis³

et al. 2017

Preprint

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Abstract:With cancer often classified as a disease that has an important epigenetic component, natural compounds that have the ability to regulate the epigenome become ideal candidates for study. Humans have a complex diet, which illustrates the need to elucidate the mechanisms of interaction between these bioactive compounds in combination. The natural compounds withaferin A (WA), from the Indian winter cherry, and sulforaphane (SFN), from cruciferous vegetables, have numerous anti-cancer effects and some report their ability to regulate epigenetic processes. Our study is the first to investigate the combinatorial effects of low physiologically achievable concentrations of WA and SFN on breast cancer cell proliferation, histone deacetylase1 (HDAC1) and DNA methyltransferases (DNMTs). No adverse effects were observed on control cells at optimal concentrations. There was synergistic inhibition of cellular viability in MCF-7 cells and a greater induction of apoptosis with the combinatorial approach than with either compound administered alone in both MDA-MB-231 and MCF-7 cells. HDAC expression was down-regulated at multiple levels. Lastly, we determined the combined effects of these bioactive compounds on the pro-apoptotic BAX and anti-apoptotic BCL-2 and found decreases in BCL-2 and increases in BAX. Taken together, our findings demonstrate the ability of low concentrations of combinatorial WA and SFN to promote cancer cell death and regulate key epigenetic modifiers in human breast cancer cells.

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Section: Discussionmentioning

confidence: 99%

Novel Combination of Withaferin A and Sulforaphane Inhibits Epigenetic Machinery, Cellular Viability and Induces Apoptosis of Breast Cancer Cells

Royston¹,

Udayakumar²,

Lewis³

et al. 2017

Preprint

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“…Various studies have also shown its cytotoxicity towards various cancer cells (Pacini et al, 1999;Strouch et al, 2009;Hastak et al, 2010). However, it was found to have cytotoxic effects against normal cells also (Sharma et al, 2011). Therefore, combinational treatment modalities using conventional therapies such as chemotherapy and newer strategies like chemoprevention are gaining attention.…”

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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“…The chemoprevention properties of glucosinolates is thought to be initiated by the isothiocyanates over a series of mechanisms including a decrease in the availability of the reactive intermediates of chemical carcinogens, suppression of cell proliferation and induction of apoptosis (Zhang, 2004). Gene expression analysis on apoptosis and inflammation showed significant down-regulation of Bcl-2, COX-2 and IL-1β after treating of HeLa cells with sulforaphane (Sharma et al, 2011). In other study, sulforaphane also induced cytotoxicity and lysosome-and mitochondria-dependent cell death in colon cancer cells with deleted p53, a tumour suppressor protein (Rudolf and Cervinka, 2011).…”

Section: Sulforaphane Is Superior To Glucoraphanin In Modulating Carcmentioning

confidence: 99%

Sulforaphane is Superior to Glucoraphanin in Modulating Carcinogen-Metabolising Enzymes in Hep G2 Cells

Razis

Noor²

2013

Asian Pacific Journal of Cancer Prevention

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Glucoraphanin is the main glucosinolate found in broccoli and other cruciferous vegetables (Brassicaceae). The objective of the study was to evaluate whether glucoraphanin and its breakdown product sulforaphane, are potent modulators of various phase I and phase II enzymes involved in carcinogen-metabolising enzyme systems in vitro. The glucosinolate glucoraphanin was isolated from cruciferous vegetables and exposed to human hepatoma cell line HepG2 at various concentrations (0-25 µM) for 24 hours. Glucoraphanin at higher concentration (25 µM) decreased dealkylation of methoxyresorufin, a marker for cytochrome P4501 activity; supplementation of the incubation medium with myrosinase (0.018 U), the enzyme that converts glucosinolate to its corresponding isothiocyanate, showed minimal induction in this enzyme activity at concentration 10 µM. Quinone reductase and glutathione S-transferase activities were unaffected by this glucosinolate; however, supplementation of the incubation medium with myrosinase elevated quinone reductase activity. It may be inferred that the breakdown product of glucoraphanin, in this case sulforaphane, is superior than its precursor in modulating carcinogenmetabolising enzyme systems in vitro and this is likely to impact on the chemopreventive activity linked to cruciferous vegetable consumption.

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Anti-carcinogenic effects of sulforaphane in association with its apoptosis-inducing and anti-inflammatory properties in human cervical cancer cells

Cited by 53 publications

References 58 publications

Novel Combination of Withaferin A and Sulforaphane Inhibits Epigenetic Machinery, Cellular Viability and Induces Apoptosis of Breast Cancer Cells

Novel Combination of Withaferin A and Sulforaphane Inhibits Epigenetic Machinery, Cellular Viability and Induces Apoptosis of Breast Cancer Cells

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

Sulforaphane is Superior to Glucoraphanin in Modulating Carcinogen-Metabolising Enzymes in Hep G2 Cells

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