Inhibition of 12-O-tetradecanoylphorbol-13-acetate-induced induction in Epstein-Barr virus early antigen in Raji cells

Okamoto, Hitoshi; Yoshida, Daisuke; Mizusaki, Shigenobu

doi:10.1016/0304-3835(83)90134-9

Cited by 48 publications

(29 citation statements)

References 7 publications

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“…Many compounds that are active in the EBV-EA assay have been confirmed to be inhibitors of tumor promotion in two-stage carcinogenesis tests in vivo. 15) Stevioside did not inhibit the induction of EBV-EA by TPA, 5) although stevioside inhibited TPA-induced inflammatory ear edema in mice. These results suggested that the assay of the inhibitory effect against TPAinduced inflammation in mouse skin was better than the assay of EBV-EA induction by TPA.…”

Section: Discussionmentioning

confidence: 95%

Inhibitory Effect of Stevioside on Tumor Promotion by 12-O-Tetradecanoylphorbol-13-acetate in Two-Stage Carcinogenesis in Mouse Skin.

Yasukawa

Kitanaka

Seo³

2002

Biological & Pharmaceutical Bulletin

131

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The leaves of Stevia rebaudiana BERTONI (Compositae), known colloquially as Caa-ehe, have been used for centuries by the Paraguayan Indians as a sweetening agent with maté tea.1) The steviol (ent-kaurene type diterpene) glycosides, stevioside, rebaudiosides A, C, and F, and dulcoside A have been isolated from S. rebaudiana and are widely used as sweeteners.2,3) In a previous paper we reported the inhibitory effect of the methanol extract of S. rebaudiana and its active component, lupeol palmitate, on inflammatory ear edema caused by 12-O-tetradecanoylphorbol-13-acetate (TPA) in mouse skin.4) Steviol inhibited Epstein-Barr virus early antigen (EBV-EA) induced by TPA in Raji cells, although stevioside did not inhibit the induction of EBV-EA by TPA.5) In this paper we examine the antiinflammatory effect of steviol glycosides, stevioside, rebaudiosides A and C and dulcoside A against TPA-induced inflammation and found these compounds to possess a marked inhibitory effect. The 50% inhibitory dose (ID 50 ) of these compounds for TPA-induced inflammation was 54.1-291.6 mg/ear. Furthermore, the stevioside mixture (the steviol glycosides from S. rebaudiana) was found to suppress markedly the tumor-promoting effect of TPA on skin tumor formation initiated with 7,12-dimethylbenz[a]anthracene (DMBA) in mouse skin. MATERIALS AND METHODSChemicals Stevioside, rabaudiosides A and C, dulcoside A, and stevioside mixture was obtained from Tokiwa Phytochemical (Chiba, Japan). These compounds were identified by chromatographic and spectroscopic comparison with authentic samples.6) The stevioside mixture contained stevioside (48.9%), rebaudioside A (24.4%), rebaudioside C (9.8%), dulcoside A (5.6%), and unidentified components (11.3%). DMBA, indomethacin, hydrocortisone, quercetin, and dimethylsulfoxide were purchased from Sigma Chemical (St. Louis, MO, U.S.A.). TPA was obtained from Chemicals for Cancer Research (Minneapolis, MN, U.S.A.).Animals Female ICR mice (7 weeks old) were obtained from the Japan SLC (Shizuoka, Japan). The animals were housed in an air-conditioned specific pathogen-free room (22-23°C), lit from 08:00 to 20:00. Food and water were available ad libitum.Assay of TPA-Induced Inflammation TPA (1 mg/ear) dissolved in acetone (20 ml) was applied to the right ear only of ICR mice using a micropipette. A volume of 10 ml was delivered to both the inner and outer surfaces of the ear. The sample, or its vehicle (20 ml), chloroform-methanol-water (1 : 2 : 1) or methanol-water (1 : 1), as a control, was applied topically about 30 min before each TPA treatment. For thickness determinations, a pocket thickness gauge (Mitsutoyo, Tokyo, Japan) with a range of 0-9 mm, graduated at 0.01-mm intervals and modified so that the contact surface area was increased to reduce the tension, was applied to the tip of the ear.The ear thickness was measured before treatment (a). Edema was measured 6 h after TPA treatment (b: TPA alone; bЈ: TPA plus sample). The following values were then calculated: Pharmacy, Nihon University; 7-7-1 Narash...

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Section: Discussionmentioning

confidence: 95%

Inhibitory Effect of Stevioside on Tumor Promotion by 12-O-Tetradecanoylphorbol-13-acetate in Two-Stage Carcinogenesis in Mouse Skin.

Yasukawa

Kitanaka

Seo³

2002

Biological & Pharmaceutical Bulletin

131

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“…Glycyrrhetinic acid was proven to inhibit the Epstein-Barr virus associated early antigen induction, ornithine decarboxylase and phospholipid metabolism controlled by tumor promoters (36)(37)(38)(39). Further studies showed that glycyrrhetinic acid could also inhibit the tumor promoting activity of 12-O-tetradecanoylphorbol-13-acetate and teleocidin in mouse skin (36).…”

Section: Discussionmentioning

confidence: 99%

18α-glycyrrhetinic acid targets prostate cancer cells by down-regulating inflammation-related genes

Munirathinam

2011

Int J Oncol

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Abstract. Glycyrrhetinic acid is an active triterpenoid metabolite of glycyrrhizin abundantly present in licorice roots. Glycyrrhetinic acid exists as α and β stereo-isomeric forms. Both stereo-isomeric forms are known to have anti-inflammatory and anticancer activity. However, the effects and anticancer mechanism of α glycyrrhetinic acid in prostate cancer cells has not yet been evaluated. Therefore, we investigated the growth inhibition, induction of apoptosis and the anticancer mechanisms of 18α-glycyrrhetinic acid (AGA), on the androgen-independent metastatic prostate cancer cell line DU-145. Our results showed that AGA inhibited proliferation and growth of these cells by inducing apoptosis as determined by Annexin V and flow cytometry analyses. Our studies also showed that HUVEC tube formation was drastically reduced when cultured in conditioned medium of AGA-treated DU-145 cells. In addition, AGA treatment prevented the invasion of DU-145 prostate cancer cells on matrigel coated transwells via down-regulation of NF-κB (p65), VEGF and MMP-9 expression. Furthermore, AGA treatment also downregulated the expression of pro-inflammatory cytokine/growth factor genes HMGB1, IL-6 and IL-8 in DU-145 cells. Interestingly, AGA simultaneously upregulated the expression of non-steroidal anti-inflammatory gene-1 (NAG-1) in DU-145 cells suggesting its anti-inflammatory activity on prostate cancer cells. Taken together, the results of this study suggest that AGA may be a promising anticancer agent that merits further investigation for the chemoprevention and treatment of prostate cancer.

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“…Recently, we [7,10] and other investigators [11,12] found that glycyrrhetic acid had inhibitory effects on TPA-induced tumor growth in vitro and in vivo. Thus, glycyrrhctic acid may be useful for chemoprevcntion during the tumor-promoting stage of carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

“…We have recently found that glycyrrhetic acid, which was shown to inhibit the induction of EpsteinBarr virus-associated early antigen and ornithine de carboxylase by 12-0-tetradecanoylphorbol-13-acctate (TPA), a tumor promoter [11,12], is also a potent inhibitor of phospholipid metabolism [10] and of hexose transport [7] stimulated by tumor promoters in vitro. Furthermore, the agent has antitumor-promot ing activity in mouse skin tumor formation induced by 7,12-dimethylbenz[a]anthracene plus teleocidin [10].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of the Specific Binding of 12-O-Tetradecanoylphorbol-13-Acetate to Mouse Epidermal Membrane Fractions by Glycyrrhetic Acid

Kitagawa¹,

Nishino²,

Iwashima³

1986

Oncology

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Glycyrrhetic acid inhibited the specific binding of 12–O–tetradecanoylphorbol-13-acetate (TPA) to mouse epidermal membrane fractions in a dose- and time-dependent manner. Glycyrrhizic acid, a glycoside of glycyrrhetic acid, has no inhibitory effect on TPA binding. The results of kinetic analysis suggested that glycyrrhetic acid directly binds to the TPA receptor, resulting in the competitive inhibition of the binding of TPA to its receptor without affecting the number of binding sites (Ki = 2.2 x 10^-4M). The inhibitory effect of glycyrrhetic acid on TPA binding to the membrane receptor may play a role in its antitumor-promoting activity in vivo.

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Inhibition of 12-O-tetradecanoylphorbol-13-acetate-induced induction in Epstein-Barr virus early antigen in Raji cells

Cited by 48 publications

References 7 publications

Inhibitory Effect of Stevioside on Tumor Promotion by 12-O-Tetradecanoylphorbol-13-acetate in Two-Stage Carcinogenesis in Mouse Skin.

Inhibitory Effect of Stevioside on Tumor Promotion by 12-O-Tetradecanoylphorbol-13-acetate in Two-Stage Carcinogenesis in Mouse Skin.

18α-glycyrrhetinic acid targets prostate cancer cells by down-regulating inflammation-related genes

Inhibition of the Specific Binding of 12-O-Tetradecanoylphorbol-13-Acetate to Mouse Epidermal Membrane Fractions by Glycyrrhetic Acid

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