Role of Ca(2+) in diallyl disulfide-induced apoptotic cell death of HCT-15 cells

Park, Eunkyung; Kwon, Kang‐Beom; Park, Kwie-In; Park, Byung‐Hyun; Jhee, Eun-Chung

doi:10.1038/emm.2002.35

Cited by 86 publications

(46 citation statements)

References 35 publications

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“…22,23,24 Both pathological increase of Ca 2 þ concentration in the cytosol compartment by inophores 25 and depletion of intracellular Ca 2 þ stores may trigger apoptosis by disrupting intracellular architecture and allowing effectors to gain access to their substrates. 24,26,27 Activation of apoptotic endonucleases 28 eliciting DNA cleavage and chromatin condensation has been well documented. 29,30,31 A tight buffering of intracellular Ca 2 þ is required for normal growth.…”

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“…29,30,31 A tight buffering of intracellular Ca 2 þ is required for normal growth. In fact, apoptosis can be induced by Ca 2 þ mobilization from intracellular pools, 23,24,27 chelation of intracellular Ca 2 þ with 1,2-bis-(2-aminophenoxy)ethane-N,N,N 1 ,N 1 -tetra-acetic acid tetra-acetoxymethyl ester (BAPTA-AM) 28,29 or removal of extracellular Ca 2 þ . 32 Intracellular Ca 2 þ deficiency regulates gene expression 22,26 and induces apoptosis through caspases activation.…”

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confidence: 99%

“…To assess whether intracellular Ca 2 þ depletion would per se cause apoptosis, we cultured PNT1A cells in the presence of BAPTA-AM, a well-known intracellular Ca 2 þ blocker 26 that can trigger activation of caspases and apoptosis. 23,28,29,33 Cell proliferation was assessed by crystal violet staining method in the presence of 20 mM BAPTA-AM. As soon as 4 h after treatment, cells growth was significantly inhibited reaching about 55 and 78% inhibition at 24 and 48 h (Po0.01, data not shown), respectively, in strict association with chromatin condensation and fragmentation, cell rounding and detachment, hallmarks of anoikis (see Figure 1e, RPMI þ BAPTA-AM).…”

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Ca2+ depletion induces nuclear clusterin, a novel effector of apoptosis in immortalized human prostate cells

et al. 2004

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Clusterin (CLU) is a secreted heterodimeric glycoprotein thatcan be produced almost ubiquitously in mammalians tissues.1Its gene expression is subjected to complex regulation and canchange enormously according to different stimuli.2 Cloned andidentified as the most potently induced gene in the regressingrat ventral prostate following androgen-ablation,3 CLU wasalmost simultaneously characterized and isolated by differentresearch groups working in widely divergent areas.2 CLU iscoded by a single copy gene, located on chromosome 8.4 Thegene codes for an initial precursor peptide glycosylated andcleaved into two a and b chains of 40 kDa each, held togetherby a unique five disulfide bond motif in the extracellular matureform.1 This secreted form of CLU has been suggested to act asa molecular chaperone following stress-induced injury,5clearing extracellular debris.6 However, it has been reportedthe existence of an inactive, cytoplasmic form of CLUproduced by alternative splicing that is converted by ionizingirradiation to a truncated mature nuclear isoform,7 which bindsthe Ku70/Ku80 complex in cell-free systems8 inhibiting cellgrowth and survival7 probably by a caspase-3-independentmechanism.9 Other alternative CLU isoforms, produced eitherby exon skipping10 or by post-translational modificationsactivated by apoptosis,11,12 were recently described. Thesedifferent isoforms of CLU have been suggested to beantiapoptotic6,13 or proapoptotic.7,10,12,14–16These controversial reports on the role of CLU might berelated to specific proteomic profiles that are produced bydifferent apoptotic stimuli (i.e. the general protein pattern ofCLU and the relative ratio between different CLU isoforms).This might explain why CLU has been involved in a plethora ofpathophysiological processes, including cell–cell and cell–matrix adhesion, cell differentiation, transformation, aging17,18and cancer,19 but its biological role still remains to be clearlyestablished. Reports suggesting that CLU may be a potentialtumor suppressor gene include the finding that CLU suppressesNF-kB activity and the metastatic phenotype ofneuroblastoma cells.20 We have previously reported that CLUoverexpression inhibits cell cycle progression of simian virus40(SV40)-immortalized human prostate PNT2 and PNT1Aepithelial cells.21To further assess the role of CLU in apoptotic processes wehave studied its expression pattern during the regulation ofcalcium homeostasis. Ca2þ is an important regulator ofapoptosis and cell survival.22,23,24 Both pathological increaseof Ca2þ concentration in the cytosol compartment byinophores25 and depletion of intracellular Ca2þ stores maytrigger apoptosis by disrupting intracellular architecture andallowing effectors to gain access to their substrates.24,26,27Activation of apoptotic endonucleases28 eliciting DNA cleavageand chromatin condensation has beenwell documented.29,30,31A tight buffering of intracellular Ca2þ is required for normalgrowth. In fact, apoptosis can be induced by Ca2þ mobilizationfrom intracellular pools,23,24,27 chelati...

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Ca2+ depletion induces nuclear clusterin, a novel effector of apoptosis in immortalized human prostate cells

et al. 2004

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“…recent studies have reported that the ability of dadS to up-or down-regulate the mrna expression of some genes is related to its signal pathway (17)(18)(19)(20)46). our results revealed that dadS may be involved in mediating multiple signal pathways in HT-29 cells by up-regulating the expression of GPCR175, GNB1, PSMD12, S100A6, TACSTD2 or by suppressing ATP1A1, YWHAE and FLJ25150 fis.…”

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confidence: 55%

“…dadS induces the elevation of cytosolic ca 2+ and activates the cell apoptotic program (18,19). in the present study, four genes, including S100 a6, TacSTd2, PABP (found in DHUG) and DNCL1 (found in DHDG), were potentially related to cell apoptosis and cytosolic ca 2+ .…”

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confidence: 99%

Diallyl disulfide inhibits the proliferation of HT-29 human colon cancer cells by inducing differentially expressed genes

Huang

Xie

et al. 2011

Mol Med Rep

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Abstract. diallyl disulfide (dadS), a sulfur compound derived from garlic, has been shown to have protective effects against colon carcinogenesis in several studies performed in rodent models. However, its molecular mechanism of action remains unclear. This study was designed to confirm the antiproliferative activity of dadS and to screen for differentially expressed genes induced by dadS in human colon cancer cells with the aim of exploring its possible anticancer mechanisms. The anti-proliferative capability of dadS in the HT-29 human colon cancer cells was analyzed by MTT assays and flow cytometry. The differences in gene expression between dadStreated (experimental group) and untreated (control group) HT-29 cells were identified using two-directional suppression subtractive hybridization (SSH). Semi-quantitative reverse transcription polymerase chain reaction (semi-rT-Pcr) was selected to confirm the results obtained by SSH. Based on the results, a dose-and time-dependent growth inhibition was observed in the dadS-treated HT-29 cells. Forty-nine known genes and a new gene were found to be involved in the anti-proliferative effects of dadS by SSH analysis, and two cdna libraries, dHdG and dHuG, containing both up-and down-regulated genes in colon tumor cells, were constructed. These genes were related to transduction, cell proliferation/ growth/apoptosis and secreted/extracellular matrix proteins. Semi-rT-Pcr results showed an expression pattern consistent with that of the SSH analysis. in conclusion, dadS showed anti-proliferative effects on colon cancer HT-29 cells, and dHdG and dHuG genes were found to be involved in this process. Further studies on the identification and description of these genes may allow a better understanding of the protective roles of dadS in colon carcinogenesis. Introductioncolon cancer is one of the major causes of cancer death worldwide (1). an understanding of the mechanisms involved in the occurrence and development of colon cancer would aid in its therapy. epidemiological investigations have provided compelling evidence that environmental factors are modifiers in colon cancer (1-3); diet has also been shown to be an important determinant of cancer risk and tumor behavior (3-5).Garlic consumption is very popular all over the world. epidemiological studies have shown an inverse correlation between the consumption of garlic and colon cancer in certain areas (6). Many in vivo experiments have revealed the antitumorigenic activity of garlic or of allyl sulfur compounds from garlic (7-17).Diallyl disulfide (DADS) is the major component of cooked garlic and an oil-soluble organosulfur compound in processed garlic that inhibits the proliferation of several human cancer cells, including breast (11), hepatoma (12), colon cancer (13) and human leukemia . Previous studies from our laboratory revealed that dadS suppresses gastric (15) and colon cancer (16). additionally, leukemia cell proliferation was related to dadS (14,17), possibly because of its ability to induce cell cycle arrest and...

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Apoptosis induction by sulfur‐containing compounds in malignant and nonmalignant human cells

Fimognari

Lenzi

Hrelia

2009

Environ and Mol Mutagen

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Plants have traditionally represented a main source for the discovery of many biologically active substances with therapeutic values. Sulfur-containing compounds exhibit pleiotropic biological effects supporting their potential use in multitargeted cancer prevention and treatment. As potential anti-cancer agents, they have been shown to inhibit or retard the growth of various cancer cells in culture and implanted tumors in vivo. The compounds significantly inhibit experimental tumorigenesis in a wide range of animal models. A critical and well-elucidated cellular mechanism involved in the anticancer activities of sulfur-containing compounds is the induction of apoptosis through the fine-tuning of orchestrated intracellular signal transduction. This review summarizes the established proapoptotic activities of sulfur-containing compounds in malignant and nonmalignant cells with a special focus on their molecular mechanisms. The potential toxicological implications of proapoptotic effects on normal cells will also be discussed.

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Role of Ca(2+) in diallyl disulfide-induced apoptotic cell death of HCT-15 cells

Abstract: Diallyl disulfide (DADS) induced apoptosis through the caspase-3 dependent pathway in leukemia cells was earlier reported from this laboratory. In this study, we investigated the involvement of Ca 2+ in DADS-induced apoptotic cell death of HCT-15, human colon cancer cell line.

Cited by 86 publications

References 35 publications

Ca2+ depletion induces nuclear clusterin, a novel effector of apoptosis in immortalized human prostate cells

Ca2+ depletion induces nuclear clusterin, a novel effector of apoptosis in immortalized human prostate cells

Diallyl disulfide inhibits the proliferation of HT-29 human colon cancer cells by inducing differentially expressed genes

Apoptosis induction by sulfur‐containing compounds in malignant and nonmalignant human cells

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