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James E Trosko - One of the best experts on this subject based on the ideXlab platform.

  • inhibition of gap junctional Intercellular Communication and activation of mitogen activated protein kinase by tumor promoting organic peroxides and protection by resveratrol
    Nutrition and Cancer, 2007
    Co-Authors: Brad L Upham, Miodrag Guzvic, Jacob Scott, Joseph M Carbone, Ludek Blaha, Lan Lan Li, Alisa M Rummel, James E Trosko
    Abstract:

    Abstract Dicumyl peroxide (di-CuOOH) and benzoyl peroxide (BzOOH) act as tumor promoters in SENCAR mice, whereas di-tert-butylhydroperoxide does not. Tumor promotion requires the removal of growth suppression by inhibition of gap junctional Intercellular Communication (GJIC) and the induction of mitogenic intracellular pathways. We showed that di-CuOOH and BzOOH both reversibly inhibited GJIC and transiently activated mitogen-activated protein kinase, specifically, the extracellular receptor kinase at noncytotoxic conditions in WB-F344 rat liver epithelial cells, whereas the non–tumor-promoting di-tert-butylhydroperoxide did not inhibit GJIC or activate extracellular receptor kinase. di-CuOOH but not BzOOH inhibited GJIC through a phosphatidylcholine-specific phospholipase C–dependent mechanism. N-Acetylcysteine (NAC) was needed to prevent a cytotoxic, glutathione-depleting effect of BzOOH, whereas di-CuOOH was noncytotoxic and did not alter glutathione levels at all doses and times tested. Pretreatment o...

  • beta sitosterol from psyllium seed husk plantago ovata forsk restores gap junctional Intercellular Communication in ha ras transfected rat liver cells
    Nutrition and Cancer, 2005
    Co-Authors: Yasushi Nakamura, Chiacheng Chang, Noriko Yoshikawa, Ikumi Hiroki, Kenji Sato, Kozo Ohtsuki, Brad L Upham, James E Trosko
    Abstract:

    We purified compounds from the husks of psyllium seeds (Plantago ovata Forsk; desert Indian wheat), beginning with an ethanol extraction then followed by HP-20 and silica gel chromatography, which restored gap junctional Intercellular Communication (GJIC) in v-Ha-ras transfected rat liver epithelial WB-F344 cell line (WB-Ha-ras). GJIC was assessed by a scrape loading dye transfer assay. The active compound was identified as beta-sitosterol based on gas chromatography retention times and electron ionization mass spectroscopy (EI-MS) spectrum of authentic beta-sitosterol. Authentic beta-sitosterol restored GJIC in the tumorigenic WB-Ha-ras GJIC-deficient cells at a dose of 2.4 micromolar. In addition, a similar phytosterol, stigmasterol, also restored GJIC, albeit at a lower activity. beta-sitosterol and stigmasterol increased the level of connexin43 protein (Cx43) and restored phosphorylation of Cx43 to levels similar to the parental nontransfected cell line. We concluded that the restoration of Intercellular Communication in the GJIC-deficient, tumorigenic WB-Ha-ras cell line by the ethanol soluble fraction of psyllium seed husks is largely due to the presence of the phytosterol, beta-sitosterol. We discuss implications for dietary modulation of cancer by beta-sitosterol.

  • β sitosterol from psyllium seed husk plantago ovata forsk restores gap junctional Intercellular Communication in ha ras transfected rat liver cells
    Nutrition and Cancer, 2005
    Co-Authors: Yasushi Nakamura, Chiacheng Chang, Noriko Yoshikawa, Ikumi Hiroki, Kenji Sato, Kozo Ohtsuki, Brad L Upham, James E Trosko
    Abstract:

    We purified compounds from the husks of psyllium seeds (Plantago ovata Forsk; desert Indian wheat), beginning with an ethanol extraction then followed by HP-20 and silica gel chromatography, which restored gap junctional Intercellular Communication (GJIC) in v-Ha-ras transfected rat liver epithelial WB-F344 cell line (WB-Ha-ras). GJIC was assessed by a scrape loading dye transfer assay. The active compound was identified as beta-sitosterol based on gas chromatography retention times and electron ionization mass spectroscopy (EI-MS) spectrum of authentic beta-sitosterol. Authentic beta-sitosterol restored GJIC in the tumorigenic WB-Ha-ras GJIC-deficient cells at a dose of 2.4 micromolar. In addition, a similar phytosterol, stigmasterol, also restored GJIC, albeit at a lower activity. beta-sitosterol and stigmasterol increased the level of connexin43 protein (Cx43) and restored phosphorylation of Cx43 to levels similar to the parental nontransfected cell line. We concluded that the restoration of Intercellular Communication in the GJIC-deficient, tumorigenic WB-Ha-ras cell line by the ethanol soluble fraction of psyllium seed husks is largely due to the presence of the phytosterol, beta-sitosterol. We discuss implications for dietary modulation of cancer by beta-sitosterol.

  • restoration of gap junctional Intercellular Communication by caffeic acid phenethyl ester cape in a ras transformed rat liver epithelial cell line
    Cancer Letters, 2000
    Co-Authors: Hyekyung Na, Chiacheng Chang, Kyungsun Kang, Melinda R Wilson, Dezider Grunberger, James E Trosko
    Abstract:

    Abstract Caffeic acid phenethyl ester (CAPE), an active ingredient of honeybee propolis, has been identified as having anti-inflammatory, anti-viral and anti-cancer properties. Since the deficiency of gap junctional Intercellular Communication (GJIC) has been shown to be a characteristic of most cancer cells, this study was designed to test the hypothesis that the anti-carcinogenic activity of CAPE might be related to its ability to restore GJIC in tumorigenic GJIC-deficient cells (WB-ras2 cells). The results showed that CAPE restored GJIC, phosphorylation of connexin 43 (Cx43) and its normal localization on the plasma membrane in WB-ras2 cells after 3 days at 5 μg/ml concentration. Additionally, CAPE inhibited growth in soft agar and decreased the protein level of p21 ras . The results are consistent with the hypothesis that the anti-cancer mechanism of CAPE may be mediated by its ability to restore GJIC.

  • in vitro growth inhibition of neoplastically transformed cells by non transformed cells requirement for gap junctional Intercellular Communication
    Carcinogenesis, 1995
    Co-Authors: Canan B Esinduy, Chiacheng Chang, James E Trosko, Randall J Ruch
    Abstract:

    : We examined whether the inhibition of neoplastically transformed cell growth by co-cultured non-transformed cells involved gap junctional Intercellular Communication (GJIC). The growth of poorly communicating (approximately 25-35% dye-coupled cells), Ha-ras and neu oncogene-transformed WB-F344 rat liver epithelial cells was inhibited by co-culture with highly communicating (90-95% dye-coupling), non-transformed WB-F344 cells. Inhibition was dependent upon heterologous cell-cell contact and required that the non-transformed cells were GJIC competent. GJIC-deficient mutant WB-F344 cells did not suppress transformed cell growth. Restoration of mutant cell GJIC by transfection with rat connexin43 cDNA restored growth-inhibiting activity. These results clearly demonstrate a role for GJIC in the inhibition of transformed cell growth by non-transformed cells.

Chiacheng Chang - One of the best experts on this subject based on the ideXlab platform.

  • beta sitosterol from psyllium seed husk plantago ovata forsk restores gap junctional Intercellular Communication in ha ras transfected rat liver cells
    Nutrition and Cancer, 2005
    Co-Authors: Yasushi Nakamura, Chiacheng Chang, Noriko Yoshikawa, Ikumi Hiroki, Kenji Sato, Kozo Ohtsuki, Brad L Upham, James E Trosko
    Abstract:

    We purified compounds from the husks of psyllium seeds (Plantago ovata Forsk; desert Indian wheat), beginning with an ethanol extraction then followed by HP-20 and silica gel chromatography, which restored gap junctional Intercellular Communication (GJIC) in v-Ha-ras transfected rat liver epithelial WB-F344 cell line (WB-Ha-ras). GJIC was assessed by a scrape loading dye transfer assay. The active compound was identified as beta-sitosterol based on gas chromatography retention times and electron ionization mass spectroscopy (EI-MS) spectrum of authentic beta-sitosterol. Authentic beta-sitosterol restored GJIC in the tumorigenic WB-Ha-ras GJIC-deficient cells at a dose of 2.4 micromolar. In addition, a similar phytosterol, stigmasterol, also restored GJIC, albeit at a lower activity. beta-sitosterol and stigmasterol increased the level of connexin43 protein (Cx43) and restored phosphorylation of Cx43 to levels similar to the parental nontransfected cell line. We concluded that the restoration of Intercellular Communication in the GJIC-deficient, tumorigenic WB-Ha-ras cell line by the ethanol soluble fraction of psyllium seed husks is largely due to the presence of the phytosterol, beta-sitosterol. We discuss implications for dietary modulation of cancer by beta-sitosterol.

  • β sitosterol from psyllium seed husk plantago ovata forsk restores gap junctional Intercellular Communication in ha ras transfected rat liver cells
    Nutrition and Cancer, 2005
    Co-Authors: Yasushi Nakamura, Chiacheng Chang, Noriko Yoshikawa, Ikumi Hiroki, Kenji Sato, Kozo Ohtsuki, Brad L Upham, James E Trosko
    Abstract:

    We purified compounds from the husks of psyllium seeds (Plantago ovata Forsk; desert Indian wheat), beginning with an ethanol extraction then followed by HP-20 and silica gel chromatography, which restored gap junctional Intercellular Communication (GJIC) in v-Ha-ras transfected rat liver epithelial WB-F344 cell line (WB-Ha-ras). GJIC was assessed by a scrape loading dye transfer assay. The active compound was identified as beta-sitosterol based on gas chromatography retention times and electron ionization mass spectroscopy (EI-MS) spectrum of authentic beta-sitosterol. Authentic beta-sitosterol restored GJIC in the tumorigenic WB-Ha-ras GJIC-deficient cells at a dose of 2.4 micromolar. In addition, a similar phytosterol, stigmasterol, also restored GJIC, albeit at a lower activity. beta-sitosterol and stigmasterol increased the level of connexin43 protein (Cx43) and restored phosphorylation of Cx43 to levels similar to the parental nontransfected cell line. We concluded that the restoration of Intercellular Communication in the GJIC-deficient, tumorigenic WB-Ha-ras cell line by the ethanol soluble fraction of psyllium seed husks is largely due to the presence of the phytosterol, beta-sitosterol. We discuss implications for dietary modulation of cancer by beta-sitosterol.

  • restoration of gap junctional Intercellular Communication by caffeic acid phenethyl ester cape in a ras transformed rat liver epithelial cell line
    Cancer Letters, 2000
    Co-Authors: Hyekyung Na, Chiacheng Chang, Kyungsun Kang, Melinda R Wilson, Dezider Grunberger, James E Trosko
    Abstract:

    Abstract Caffeic acid phenethyl ester (CAPE), an active ingredient of honeybee propolis, has been identified as having anti-inflammatory, anti-viral and anti-cancer properties. Since the deficiency of gap junctional Intercellular Communication (GJIC) has been shown to be a characteristic of most cancer cells, this study was designed to test the hypothesis that the anti-carcinogenic activity of CAPE might be related to its ability to restore GJIC in tumorigenic GJIC-deficient cells (WB-ras2 cells). The results showed that CAPE restored GJIC, phosphorylation of connexin 43 (Cx43) and its normal localization on the plasma membrane in WB-ras2 cells after 3 days at 5 μg/ml concentration. Additionally, CAPE inhibited growth in soft agar and decreased the protein level of p21 ras . The results are consistent with the hypothesis that the anti-cancer mechanism of CAPE may be mediated by its ability to restore GJIC.

  • in vitro growth inhibition of neoplastically transformed cells by non transformed cells requirement for gap junctional Intercellular Communication
    Carcinogenesis, 1995
    Co-Authors: Canan B Esinduy, Chiacheng Chang, James E Trosko, Randall J Ruch
    Abstract:

    : We examined whether the inhibition of neoplastically transformed cell growth by co-cultured non-transformed cells involved gap junctional Intercellular Communication (GJIC). The growth of poorly communicating (approximately 25-35% dye-coupled cells), Ha-ras and neu oncogene-transformed WB-F344 rat liver epithelial cells was inhibited by co-culture with highly communicating (90-95% dye-coupling), non-transformed WB-F344 cells. Inhibition was dependent upon heterologous cell-cell contact and required that the non-transformed cells were GJIC competent. GJIC-deficient mutant WB-F344 cells did not suppress transformed cell growth. Restoration of mutant cell GJIC by transfection with rat connexin43 cDNA restored growth-inhibiting activity. These results clearly demonstrate a role for GJIC in the inhibition of transformed cell growth by non-transformed cells.

Brad L Upham - One of the best experts on this subject based on the ideXlab platform.

  • inhibition of gap junctional Intercellular Communication and activation of mitogen activated protein kinase by tumor promoting organic peroxides and protection by resveratrol
    Nutrition and Cancer, 2007
    Co-Authors: Brad L Upham, Miodrag Guzvic, Jacob Scott, Joseph M Carbone, Ludek Blaha, Lan Lan Li, Alisa M Rummel, James E Trosko
    Abstract:

    Abstract Dicumyl peroxide (di-CuOOH) and benzoyl peroxide (BzOOH) act as tumor promoters in SENCAR mice, whereas di-tert-butylhydroperoxide does not. Tumor promotion requires the removal of growth suppression by inhibition of gap junctional Intercellular Communication (GJIC) and the induction of mitogenic intracellular pathways. We showed that di-CuOOH and BzOOH both reversibly inhibited GJIC and transiently activated mitogen-activated protein kinase, specifically, the extracellular receptor kinase at noncytotoxic conditions in WB-F344 rat liver epithelial cells, whereas the non–tumor-promoting di-tert-butylhydroperoxide did not inhibit GJIC or activate extracellular receptor kinase. di-CuOOH but not BzOOH inhibited GJIC through a phosphatidylcholine-specific phospholipase C–dependent mechanism. N-Acetylcysteine (NAC) was needed to prevent a cytotoxic, glutathione-depleting effect of BzOOH, whereas di-CuOOH was noncytotoxic and did not alter glutathione levels at all doses and times tested. Pretreatment o...

  • β sitosterol from psyllium seed husk plantago ovata forsk restores gap junctional Intercellular Communication in ha ras transfected rat liver cells
    Nutrition and Cancer, 2005
    Co-Authors: Yasushi Nakamura, Chiacheng Chang, Noriko Yoshikawa, Ikumi Hiroki, Kenji Sato, Kozo Ohtsuki, Brad L Upham, James E Trosko
    Abstract:

    We purified compounds from the husks of psyllium seeds (Plantago ovata Forsk; desert Indian wheat), beginning with an ethanol extraction then followed by HP-20 and silica gel chromatography, which restored gap junctional Intercellular Communication (GJIC) in v-Ha-ras transfected rat liver epithelial WB-F344 cell line (WB-Ha-ras). GJIC was assessed by a scrape loading dye transfer assay. The active compound was identified as beta-sitosterol based on gas chromatography retention times and electron ionization mass spectroscopy (EI-MS) spectrum of authentic beta-sitosterol. Authentic beta-sitosterol restored GJIC in the tumorigenic WB-Ha-ras GJIC-deficient cells at a dose of 2.4 micromolar. In addition, a similar phytosterol, stigmasterol, also restored GJIC, albeit at a lower activity. beta-sitosterol and stigmasterol increased the level of connexin43 protein (Cx43) and restored phosphorylation of Cx43 to levels similar to the parental nontransfected cell line. We concluded that the restoration of Intercellular Communication in the GJIC-deficient, tumorigenic WB-Ha-ras cell line by the ethanol soluble fraction of psyllium seed husks is largely due to the presence of the phytosterol, beta-sitosterol. We discuss implications for dietary modulation of cancer by beta-sitosterol.

  • beta sitosterol from psyllium seed husk plantago ovata forsk restores gap junctional Intercellular Communication in ha ras transfected rat liver cells
    Nutrition and Cancer, 2005
    Co-Authors: Yasushi Nakamura, Chiacheng Chang, Noriko Yoshikawa, Ikumi Hiroki, Kenji Sato, Kozo Ohtsuki, Brad L Upham, James E Trosko
    Abstract:

    We purified compounds from the husks of psyllium seeds (Plantago ovata Forsk; desert Indian wheat), beginning with an ethanol extraction then followed by HP-20 and silica gel chromatography, which restored gap junctional Intercellular Communication (GJIC) in v-Ha-ras transfected rat liver epithelial WB-F344 cell line (WB-Ha-ras). GJIC was assessed by a scrape loading dye transfer assay. The active compound was identified as beta-sitosterol based on gas chromatography retention times and electron ionization mass spectroscopy (EI-MS) spectrum of authentic beta-sitosterol. Authentic beta-sitosterol restored GJIC in the tumorigenic WB-Ha-ras GJIC-deficient cells at a dose of 2.4 micromolar. In addition, a similar phytosterol, stigmasterol, also restored GJIC, albeit at a lower activity. beta-sitosterol and stigmasterol increased the level of connexin43 protein (Cx43) and restored phosphorylation of Cx43 to levels similar to the parental nontransfected cell line. We concluded that the restoration of Intercellular Communication in the GJIC-deficient, tumorigenic WB-Ha-ras cell line by the ethanol soluble fraction of psyllium seed husks is largely due to the presence of the phytosterol, beta-sitosterol. We discuss implications for dietary modulation of cancer by beta-sitosterol.

Yasushi Nakamura - One of the best experts on this subject based on the ideXlab platform.

  • β sitosterol from psyllium seed husk plantago ovata forsk restores gap junctional Intercellular Communication in ha ras transfected rat liver cells
    Nutrition and Cancer, 2005
    Co-Authors: Yasushi Nakamura, Chiacheng Chang, Noriko Yoshikawa, Ikumi Hiroki, Kenji Sato, Kozo Ohtsuki, Brad L Upham, James E Trosko
    Abstract:

    We purified compounds from the husks of psyllium seeds (Plantago ovata Forsk; desert Indian wheat), beginning with an ethanol extraction then followed by HP-20 and silica gel chromatography, which restored gap junctional Intercellular Communication (GJIC) in v-Ha-ras transfected rat liver epithelial WB-F344 cell line (WB-Ha-ras). GJIC was assessed by a scrape loading dye transfer assay. The active compound was identified as beta-sitosterol based on gas chromatography retention times and electron ionization mass spectroscopy (EI-MS) spectrum of authentic beta-sitosterol. Authentic beta-sitosterol restored GJIC in the tumorigenic WB-Ha-ras GJIC-deficient cells at a dose of 2.4 micromolar. In addition, a similar phytosterol, stigmasterol, also restored GJIC, albeit at a lower activity. beta-sitosterol and stigmasterol increased the level of connexin43 protein (Cx43) and restored phosphorylation of Cx43 to levels similar to the parental nontransfected cell line. We concluded that the restoration of Intercellular Communication in the GJIC-deficient, tumorigenic WB-Ha-ras cell line by the ethanol soluble fraction of psyllium seed husks is largely due to the presence of the phytosterol, beta-sitosterol. We discuss implications for dietary modulation of cancer by beta-sitosterol.

  • beta sitosterol from psyllium seed husk plantago ovata forsk restores gap junctional Intercellular Communication in ha ras transfected rat liver cells
    Nutrition and Cancer, 2005
    Co-Authors: Yasushi Nakamura, Chiacheng Chang, Noriko Yoshikawa, Ikumi Hiroki, Kenji Sato, Kozo Ohtsuki, Brad L Upham, James E Trosko
    Abstract:

    We purified compounds from the husks of psyllium seeds (Plantago ovata Forsk; desert Indian wheat), beginning with an ethanol extraction then followed by HP-20 and silica gel chromatography, which restored gap junctional Intercellular Communication (GJIC) in v-Ha-ras transfected rat liver epithelial WB-F344 cell line (WB-Ha-ras). GJIC was assessed by a scrape loading dye transfer assay. The active compound was identified as beta-sitosterol based on gas chromatography retention times and electron ionization mass spectroscopy (EI-MS) spectrum of authentic beta-sitosterol. Authentic beta-sitosterol restored GJIC in the tumorigenic WB-Ha-ras GJIC-deficient cells at a dose of 2.4 micromolar. In addition, a similar phytosterol, stigmasterol, also restored GJIC, albeit at a lower activity. beta-sitosterol and stigmasterol increased the level of connexin43 protein (Cx43) and restored phosphorylation of Cx43 to levels similar to the parental nontransfected cell line. We concluded that the restoration of Intercellular Communication in the GJIC-deficient, tumorigenic WB-Ha-ras cell line by the ethanol soluble fraction of psyllium seed husks is largely due to the presence of the phytosterol, beta-sitosterol. We discuss implications for dietary modulation of cancer by beta-sitosterol.

Paule Martel - One of the best experts on this subject based on the ideXlab platform.

  • flavonoids apigenin tangeretin counteract tumor promoter induced inhibition of Intercellular Communication of rat liver epithelial cells
    Cancer Letters, 1997
    Co-Authors: Catherine Chaumontet, Valerie Bex, Isabelle Gaillardsanchez, Catherine Droumaguet, Christine Heberden, Paule Martel
    Abstract:

    We have shown previously that two flavonoids, apigenin and tangeretin, enhance gap junctional Intercellular Communication (GJIC) in rat liver epithelial cells, named REL cells. Here, we show that these two flavones also antagonize the inhibition of GJIC induced by tumor promoters like 12-O-tetradecanoyl-phorbol-acetate (TPA) and 3,5,di-tertio-butyl-4-hydroxytoluene (BHT). Their preventive effect is rapid. It does not seem to involve any change of the amount of the connexin expressed in REL cells, connexin 43 (Cx 43), and in its phosphorylation state. Other flavonoids tested including naringenin, myricetin, catechin and chrysin did not enhance GJIC nor counteract TPA-induced inhibition of GJIC.

  • apigenin and tangeretin enhance gap junctional Intercellular Communication in rat liver epithelial cells
    Carcinogenesis, 1994
    Co-Authors: Catherine Chaumontet, Valerie Bex, Isabelle Gaillardsanchez, Christine Seillanheberden, Marc Suschetet, Paule Martel
    Abstract:

    Two flavones, apigenin and tangeretin, were studied for their ability to modulate gap junctional Intercellular Communication (GJIC) in the rat liver epithelial cell line REL. Their cytotoxicity was first determined by cell density and neutral red uptake assays: neither apigenin nor tangeretin are cytotoxic at 10 and 25 microM, the concentrations used in our experiments. We then studied GJIC using the dye transfer assay and we observed that both apigenin and tangeretin enhance it, the maximum stimulation (x 1.7-1.8) being achieved at 25 microM for 24 h. When the dye transfer was enhanced, the amount of connexin 43 increased, which was demonstrated by Western blot and immunofluorescence analysis. For apigenin only, Northern blot analysis showed an accumulation of connexin 43 mRNA. In addition, the incubation of REL cells with the two compounds, for 1 or 24 h, prevented the inhibition of dye transfer by 12-O-tetradecanoylphorbol-13-acetate (1 or 10 ng/ml). The enhancement of GJIC by apigenin could be one of the major mechanisms responsible for apigenin's anti-tumour promoting action in vivo. As for tangeretin, its capacity to enhance GJIC completes its potential protective properties towards the post-initiation process.