Su Yel Lee

Genistein and curcumin suppress epidermal growth factor-induced MUC5AC mucin production and gene expression from human airway epithelial cells.

This study investigated whether genistein and curcumin affect epidermal growth factor (EGF)‐induced MUC5AC mucin production and gene expression from human airway epithelial cells. Confluent NCI‐H292 cells were pretreated with each agent for 30 min and then stimulated with EGF for 24 h. The MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription – polymerase chain reaction (RT‐PCR) and enzyme‐linked immunosorbent assay (ELISA), respectively. The results were as follows: (1) genistein and curcumin inhibited the production of MUC5AC mucin protein induced by EGF, dose‐dependently; (2) genistein and curcumin also inhibited the expression of MUC5AC mucin gene induced by EGF. This result suggests that genistein and curcumin can regulate mucin gene expression and production of mucin protein induced by EGF, by directly acting on airway epithelial cells. Copyright

Inhibition of secretion, production and gene expression of mucin from cultured airway epithelial cells by prunetin.

This study investigated whether prunetin significantly affects the secretion, production and gene expression of mucin from cultured airway epithelial cells. Confluent primary rat tracheal surface epithelial (RTSE) cells were pretreated with adenosine triphosphate (ATP) for 5 min and then chased for 30 min in the presence of prunetin to assess the effect on mucin secretion using enzyme‐linked immunosorbent assay (ELISA). At the same time, confluent NCI‐H292 cells were pretreated with prunetin for 30 min and then stimulated with epidermal growth factor (EGF) or phorbol 12‐myristate 13‐acetate (PMA) for 24 h, respectively. The MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription‐polymerase chain reaction (RT‐PCR) and ELISA. The results were as follows: (1) prunetin significantly suppressed ATP‐induced mucin secretion from cultured RTSE cells; (2) prunetin inhibited the production of MUC5AC mucin protein induced by EGF or PMA from NCI‐H292 cells; (3) prunetin also inhibited the expression of MUC5AC mucin gene induced by EGF or PMA from NCI‐H292 cells. This result suggests that prunetin can regulate the secretion, production and gene expression of mucin, by directly acting on airway epithelial cells. Copyright

Silibinin Regulates Gene Expression, Production and Secretion of Mucin from Cultured Airway Epithelial Cells

We investigated whether silibinin significantly affects gene expression, production and secretion of mucin from cultured airway epithelial cells. Confluent NCI‐H292 cells were pretreated with silibinin for 30 min and then stimulated with epidermal growth factor (EGF), phorbol 12‐myristate 13‐acetate (PMA) or TNF‐α for 24 h. The MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription–polymerase chain reaction (RT‐PCR) and enzyme‐linked immunosorbent assay (ELISA). The effect of silibinin on TNF‐α‐induced activation of NF‐κB p65 was also examined. Confluent primary rat tracheal surface epithelial (RTSE) cells were pretreated with adenosine triphosphate (ATP) for 5 min and then treated for 30 min in the presence of silibinin to assess the effect on mucin secretion using ELISA. The results were as follows: (i) silibinin inhibited the expression of the MUC5AC mucin gene induced by EGF, PMA or TNF‐α from NCI‐H292 cells; (ii) silibinin also inhibited the production of MUC5AC mucin protein induced by the same inducers from NCI‐H292 cells; (iii) silibinin inhibited the activation of NF‐κB p65 by TNF‐α in NCI‐H292 cells; (iv) silibinin significantly decreased ATP‐induced mucin secretion from cultured RTSE cells. This result suggests that silibinin can regulate gene expression, production and secretion of mucin by directly acting on airway epithelial cells. Copyright

Resveratrol Inhibits Mucin Gene Expression, Production and Secretion From Airway Epithelial Cells

The study investigated whether resveratrol significantly affects mucin gene expression, production and secretion from airway epithelial cells. Confluent NCI‐H292 cells were pretreated with resveratrol for 30 min and then stimulated with EGF (epidermal growth factor), PMA (phorbol 12‐myristate 13‐acetate) and TNF‐α (tumor necrosis factor‐α) for 24 h, respectively. The MUC5AC gene expression and mucin protein production were measured by RT‐PCR and ELISA. The effect of resveratrol on TNF‐α‐ or PMA‐induced activation of NF‐κB p65 was also examined. Confluent primary rat tracheal surface epithelial (RTSE) cells were pretreated with adenosine triphosphate (ATP) for 5 min and then treated for 30 min in the presence of resveratrol to assess the effect on mucin secretion using ELISA. The results were as follows: (1) resveratrol inhibited the expression of MUC5AC gene induced by EGF or PMA or TNF‐α from NCI‐H292 cells; (2) resveratrol also inhibited the production of MUC5AC mucin protein induced by the same inducers from NCI‐H292 cells; (3) resveratrol inhibited the activation of NF‐κB p65 by TNF‐α or PMA in NCI‐H292 cells; (4) resveratrol significantly decreased ATP‐induced mucin secretion from cultured RTSE cells. This result suggests that resveratrol can regulate mucin gene expression, production and secretion, by directly acting on airway epithelial cells. Copyright

Inhibition of airway MUC5AC mucin production and gene expression induced by epidermal growth factor or phorbol ester by glycyrrhizin and carbenoxolone.

BACKGROUND AND AIM In this study, we investigated whether glycyrrhizin and carbenoxolone affect MUC5AC mucin production and gene expression induced by epidermal growth factor (EGF) or phorbol ester (PMA) from human airway epithelial cells. METHODS Confluent NCI-H292 cells were pretreated with each agent for 30 min and then stimulated with EGF and PMA for 24h, respectively. MUC5AC mucin gene expression and mucin protein production were measured by RT-PCR and ELISA. RESULTS Glycyrrhizin and carbenoxolone were found to inhibit the production of MUC5AC mucin protein induced by EGF or PMA, and both compounds also inhibited the expression of MUC5AC mucin gene induced by EGF or PMA. CONCLUSION These results suggest that glycyrrhizin and carbenoxolone can inhibit mucin gene expression and production of mucin protein, by directly acting on airway epithelial cells.

Oleanolic acid and ursolic acid derived from Cornus officinalis Sieb. et Zucc. suppress epidermal growth factor- and phorbol ester-induced MUC5AC mucin production and gene expression from human airway epithelial cells.

In this study, the effects of oleanolic acid and ursolic acid on MUC5AC mucin production and gene expression induced by epidermal growth factor (EGF) and phorbol 12‐myristate 13‐acetate (PMA) from human airway epithelial cells were investigated. Confluent NCI‐H292 cells were pretreated with each agent for 30 min and then stimulated with EGF and PMA for 24 h, respectively. MUC5AC mucin gene expression and mucin protein production were measured by RT‐PCR and ELISA. Oleanolic acid and ursolic acid were found to inhibit the production of MUC5AC mucin protein induced by EGF and PMA, and both compounds also inhibited the expression of MUC5AC mucin gene induced by EGF and PMA. These results suggest that oleanolic acid and ursolic acid can regulate mucin gene expression, and production of mucin protein, by directly acting on airway epithelial cells. Copyright

Abstract 772: Effects of natural products on proliferation of human breast cancer cells induced by estrogen or PhIP, a heterocyclic amine compound derived from cooked meat

Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC According to the traditional Asian medicine, herbs containing daidzein, hesperidin, oleanolic acid and bacalein were used as anti-inflammatory and anti-tumor folk medicines. On the basis of this information, in this study, we investigated whether natural products including daidzein, hesperidin, oleanolic acid and bacalein affect proliferation of MCF-7 human breast cancer cells stimulated by 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine (PhIP) or estradiol. The results were as follows : (1) Both estradiol and PhIP significantly induced proliferation of MCF-7 cells at the concentrations of 10nM and 100nM, respectively; (2) Oleanolic acid and baicalein inhibited proliferation of PhIP-induced proliferation of MCF-7 cells, dose-dependently; (3) Daidzein and hesperidin also inhibited proliferation of estradiol-induced proliferation of MCF-7 cells, dose-dependently. We suggest that these four natural compounds can be novel drug candidates for preventing breast cancer provoked by dietary estrogenic compounds found in cooked meat such as PhIP. Also, effects of these four natural compounds on MAPK-ERK pathway should be investigated for elucidation of action mechanism through future study. (Key words: Natural products, MCF-7, PhIP, Estradiol) Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 772.