Apoptosis induction in human lung adenocarcinoma cells by oil‐soluble allyl sulfides: Triggers, pathways, and modulators

Wu, Xuehang; Ying, Haoqiang; Lamy, Evelyn; Mersch-Sundermann, Volker

doi:10.1002/em.20467

Cited by 58 publications

(52 citation statements)

References 44 publications

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“…Although DATS failed to modulate TPA-induced p38 MAPK activation (data not shown), the compound significantly attenuated the phosphorylation and the catalytic activity of JNK in TPA-stimulated mouse skin. In contrast, DATS induces apoptosis in various cancer cells through upregulation of JNK (32,33).…”

Section: Discussionmentioning

confidence: 97%

Diallyl Trisulfide Inhibits Phorbol Ester–Induced Tumor Promotion, Activation of AP-1, and Expression of COX-2 in Mouse Skin by Blocking JNK and Akt Signaling

Shrotriya

Kundu

et al. 2010

Cancer Research

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An inverse relationship exists between the consumption of garlic and the risk of certain cancers. The present study was aimed at investigating the effect of garlic constituent diallyl trisulfide (DATS) on 12-Otetradecanoylphorbol-13-acetate (TPA)-induced cyclooxygenase-2 (COX-2) expression and tumor promotion in mouse skin and to explore the underlying molecular mechanisms. Pretreatment of mouse skin with different garlic-derived allyl sulfides showed DATS to be the most potent in suppressing TPA-induced COX-2 expression. DATS significantly attenuated the DNA binding of activator protein-1 (AP-1), one of the transcription factors that regulate COX-2 expression, in TPA-stimulated mouse skin. DATS also diminished TPA-induced expression of c-Jun and c-Fos, the principal components of AP-1, and blunted the activation of c-Jun NH 2 -terminal kinase (JNK) and Akt. Pharmacologic inhibition of JNK or Akt by SP600125 or LY294002, respectively, resulted in diminished AP-1 DNA binding, reduced levels of c-Jun and c-Fos, and inhibition of COX-2 expression in TPA-treated mouse skin. The JNK or Akt kinase assay, taking c-Jun fusion protein as a substrate, revealed that TPA induced JNK-or Akt-mediated c-Jun phosphorylation in mouse skin, which was significantly attenuated by DATS or respective pharmacologic inhibitors. Evaluation of antitumor-promoting effect of DATS on 7,12-dimethylbenz(a)anthracene-initiated and TPA-promoted mouse skin carcinogenesis showed that pretreatment with DATS significantly reduced the incidence and multiplicity of papillomas. Taken together, the inhibitory effects of DATS on TPA-induced AP-1 activation and COX-2 expression through modulation of JNK or Akt signaling may partly account for its antitumor-promoting effect on mouse skin carcinogenesis. Cancer Res; 70(5); 1932-40. ©2010 AACR.

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Section: Discussionmentioning

confidence: 97%

Diallyl Trisulfide Inhibits Phorbol Ester–Induced Tumor Promotion, Activation of AP-1, and Expression of COX-2 in Mouse Skin by Blocking JNK and Akt Signaling

Shrotriya

Kundu

et al. 2010

Cancer Research

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“…Garlic oils contain major organosulfur compounds, including diallyl sulfide (DAS; 112 g/g), diallyl disulfide (DADS; 1,183 g/g), and diallyl trisulfide (DATS; 751 g/g), and minor amounts of many other volatile compounds (49). These compounds possess potent anticancer, antioxidant, and anti-inflammatory immune modulation activities and antimicrobial properties (2,30,71,72,79,83). The inhibitory effect of DASs against Bacillus cereus, Salmonella sp., and Vibrio cholerae (7,62,63), Staphylococcus aureus and Candida albicans (42,51), Helicobacter pylori (52,58), and Klebsiella pneu-moniae and Pseudomonas aeruginosa (17,37,53,73) were studied, and a recent report has shown that DASs were synergistically effective when combined with antibiotics against antibiotic-resistant strains of Escherichia coli, Enterobacter cloacae, E. faecalis, and Citrobacter freundii (80).…”

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confidence: 99%

In Vitro Efficacy of Diallyl Sulfides against the Periodontopathogen Aggregatibacter actinomycetemcomitans

Velliyagounder

Ganeshnarayan

Velusamy

et al. 2012

Antimicrob Agents Chemother

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The in vitro antibacterial effects of diallyl sulfide (DAS) against the Gram-negative periodontopathogen Aggregatibacter actinomycetemcomitans, the key etiologic agent of the severe form of localized aggressive periodontitis and other nonoral infections, were studied. A. actinomycetemcomitans was treated with garlic extract, allicin, or DAS, and the anti-A. actinomycetemcomitans effects of the treatment were evaluated. Garlic extract, allicin, and DAS significantly inhibited the growth of A. actinomycetemcomitans (greater than 3 log; P < 0.01) compared to control cells. Heat inactivation of the garlic extracts significantly reduced the protein concentration; however, the antimicrobial effect was retained. Purified proteins from garlic extract did not exhibit antimicrobial activity. Allicin lost all its antimicrobial effect when it was subjected to heat treatment, whereas DAS demonstrated an antimicrobial effect similar to that of the garlic extract, suggesting that the antimicrobial activity of garlic extract is mainly due to DAS. An A. actinomycetemcomitans biofilm-killing assay performed with DAS showed a significant reduction in biofilm cell numbers, as evidenced by both confocal microscopy and culture. Scanning electron microscopy (SEM) analysis of DAS-treated A. actinomycetemcomitans biofilms showed alterations of colony architecture indicating severe stress. Flow cytometry analysis of OBA9 cells did not demonstrate apoptosis or cell cycle arrest at therapeutic concentrations of DAS (0.01 and 0.1 g/ml). DAStreated A. actinomycetemcomitans cells demonstrated complete inhibition of glutathione (GSH) S-transferase (GST) activity. However, OBA9 cells, when exposed to DAS at similar concentrations, showed no significant differences in GST activity, suggesting that DAS-induced GST inhibition might be involved in A. actinomycetemcomitans cell death. These findings demonstrate that DAS exhibits significant antibacterial activity against A. actinomycetemcomitans and that this property might be utilized for exploring its therapeutic potential in treatment of A. actinomycetemcomitans-associated oral and nonoral infections.

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“…The regulation of apoptosis is, therefore, the most important in the treatment of cancer (Fulda, 2010;Lawen, 2003;Reed, 2002). Accumulated evidences indicated that the most of chemotherapeutic agents halt tumor cells proliferation via induction of apoptosis (Saha et al, 2010;Wu et al, 2009;Zhang, 2002). We examined whether jaceosidin inhibited cell growth of T24 cells through the induction of apoptosis.…”

Section: Resultsmentioning

confidence: 99%

Jaceosidin inhibits proliferation of human bladder cancer T24 cells through induction of cell cycle arrest and apoptosis

Yong

Tan

2013

Bangladesh J Pharmacol

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Jaceosidin, isolated from Artemesia argyi, has been shown to possess promising anti-cancer potential against various cancer cells. However, its effect against bladder cancer cells remained unknown. In this study, for the first time, we investigated the effects of jaceosidin on cell proliferation, cell cycle, and apoptosis in bladder cancer T24 cells by using MTT assay and flow cytometric analysis. The results revealed that jaceosidin decreased the cell viability of bladder cancer T24 cells in a dose-and time-dependent manner. Flow cytometric analysis demonstrated that jaceosidin significantly triggered apoptosis in T24 cells and arrested cell cycle at G2/M phase in a timedependent manner. Further characterization showed that jaceosidin-induced apoptosis is associated with dissipation in mitochondrial membrane potential (ΔΨm), up-regulation of Bax and down-regulation of Bcl-2 in jaceosidintreated T24 cells. These in vitro results suggested that jaceosidin should be further examined for in vivo activity and molecular mechanism in human bladder cancer. Article Info

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Apoptosis induction in human lung adenocarcinoma cells by oil‐soluble allyl sulfides: Triggers, pathways, and modulators

Cited by 58 publications

References 44 publications

Diallyl Trisulfide Inhibits Phorbol Ester–Induced Tumor Promotion, Activation of AP-1, and Expression of COX-2 in Mouse Skin by Blocking JNK and Akt Signaling

Diallyl Trisulfide Inhibits Phorbol Ester–Induced Tumor Promotion, Activation of AP-1, and Expression of COX-2 in Mouse Skin by Blocking JNK and Akt Signaling

In Vitro Efficacy of Diallyl Sulfides against the Periodontopathogen Aggregatibacter actinomycetemcomitans

Jaceosidin inhibits proliferation of human bladder cancer T24 cells through induction of cell cycle arrest and apoptosis

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