• The Korean Journal of Physiology and Pharmacology
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• v.22 no.6
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• pp.671-677
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• 2018

In the present study, we investigated whether tussilagone, a natural product derived from Tussilago farfara, significantly affects the production and gene expression of airway MUC5AC mucin. Confluent NCI-H292 cells were pretreated with tussilagone for 30 min and then stimulated with EGF (epidermal growth factor) or PMA (phorbol 12-myristate 13-acetate) for 24 h or the indicated periods. The MUC5AC mucin gene expression was measured by RT-PCR. Production of MUC5AC mucin protein was measured by ELISA. To elucidate the action mechanism of tussilagone, effect of tussilagone on PMA-induced $NF-{\kappa}B$ signaling pathway was investigated by western blot analysis. Tussilagone significantly inhibited the production of MUC5AC mucin protein and down-regulated the expression of MUC5AC mucin gene, induced by EGF or PMA. Tussilagone inhibited PMA-induced activation (phosphorylation) of inhibitory kappa B kinase (IKK), and thus phosphorylation and degradation of inhibitory kappa Ba ($I{\kappa}B{\alpha}$). Tussilagone inhibited PMA-induced phosphorylation and nuclear translocation of nuclear factor kappa B ($NF-{\kappa}B$) p65. This, in turn, led to the down-regulation of MUC5AC protein production in NCI-H292 cells. These results suggest that tussilagone can regulate the production and gene expression of mucin by acting on airway epithelial cells through regulation of $NF-{\kappa}B$ signaling pathway.

• Korean Journal of Microbiology
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• v.30 no.5
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• pp.371-376
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• 1992

Plasmid pSL4 of plasmid pKM 101 mutant have high protection effects and mutagenecity for UV and methyl methanesulfonate, The mucA gene and a pan of mucE gene of pKM 101 and pSL4 were sucloned onto lacZ' fusion vector pMC874 and the hybrid plasmids pBH31 and pBH30 were selected. These plsmids were intrduced into $recA^{+}lexA^{-}$, $recA^{-}와lexA^{+}$ strains and determined the activity of $\beta$-galactosidase for UV. In $recA^{+}lexA^{+}$ strain.$\beta$-galactosidase activity of pBH30 included mue region of pSL4 was higher thall pBH31 inclued muc region of pKM 10 I and the tf-galactosidase of two plasmids was not induced in reeA and leeA mutants with or without UV illumination. Without UV illumination. the .$\beta$-galactosidasc of pBH30 was expressed a little higher level than that of pBH3L We suggest that the functional difference of pKM 10l and pSL4 are due to the variety of mue regulatory region. Also. a plasmid pBH 100 earring umuC' -lacZ' gene fusion was constructed in vitro to study the regulation of the umu operon. It was shown that the umu operon is induced by UV and is regulated by the reeA and lexA genes.

• Biomolecules & Therapeutics
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• v.19 no.3
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• pp.320-323
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• 2011

We conducted this study to investigate whether berberine signifi cantly affects MUC5AC mucin gene expression and mucin production induced by epidermal growth factor (EGF), phorbol 12-myristate 13-acetate (PMA) or tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) from human airway epithelial cells. Confl uent NCI-H292 cells were pretreated with varying concentrations of berberine for 30 min and then stimulated with EGF, PMA or TNF-${\alpha}$ for 24 h. MUC5AC mucin gene expression and mucin production were measured by reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Berberine was found to inhibit the expression of MUC5AC mucin gene induced by EGF, PMA or TNF-${\alpha}$. Berberine also inhibited the production of MUC5AC mucin protein stimulated by the same inducers. This result suggests that berberine can regulate the expression of mucin gene and production of mucin protein, by directly acting on human airway epithelial cells.

• Tuberculosis and Respiratory Diseases
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• v.69 no.5
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• pp.348-353
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• 2010

Background: In this study, we tried to investigate whether carbenoxolone, prunetin, and silibinin affect tumor necrosis factor (TNF)-${\alpha}$-induced MUC5AC mucin production and gene expression from human airway epithelial cells. Methods: Confluent NCI-H292 cells were pretreated with each agent (carbenoxolone, prunetin, and silibinin) for 30 min and then stimulated with TNF-${\alpha}$ for 24 hours. The MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription-polymerase chain reaction and enzyme linked immunosorbent assay, respectively. Results: Carbenoxolone, prunetin and silibinin inhibited the production of MUC5AC mucin protein induced by TNF-${\alpha}$; the 3 compounds also inhibited the expression of MUC5AC mucin gene induced by TNF-${\alpha}$. Conclusion: This result suggests that carbenoxolone, prunetin and silibinin can inhibit mucin gene expression and production of mucin protein induced by TNF-${\alpha}$, by directly acting on airway epithelial cells.

• Natural Product Sciences
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• v.25 no.3
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• pp.248-254
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• 2019

In the present study, we investigated whether quercitrin, quercetin and afzelin derived from Houttuynia cordata affect the production and gene expression of MUC5AC mucin from airway epithelial cells. Confluent NCI-H292 cells were pretreated with quercitrin, quercetin or afzelin for 30 min and then stimulated with epidermal growth factor (EGF) or phorbol 12-myristate 13-acetate (PMA) for 24 h. The MUC5AC mucin gene expression and production were measured by RT-PCR and ELISA, respectively. The results were as follows: (1) Quercitrin, quercetin and afzelin inhibited EGF- and PMA-induced MUC5AC mucin production from NCI-H292 cells; (2) The three natural products also decreased EGF- and PMA-induced MUC5AC mucin gene expression in NCI-H292 cells. These results suggest that quercitrin, quercetin and afzelin showed the regulatory effect on the steps of gene expression and production of mucin, by directly acting on airway epithelial cells.

• Biomolecules & Therapeutics
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• v.29 no.3
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• pp.303-310
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• 2021

In the present study, kaempferol, a flavonoidal natural compound found in Polygonati Rhizoma, was investigated for its potential effect on the gene expression and production of airway MUC5AC mucin. A human respiratory epithelial NCI-H292 cells was pretreated with kaempferol for 30 min and stimulated with epidermal growth factor (EGF) or phorbol 12-myristate 13-acetate (PMA), for the following 24 h. The effect on PMA-induced nuclear factor kappa B (NF-κB) signaling pathway or EGF-induced mitogen-activated protein kinase (MAPK) signaling pathway was investigated. Kaempferol suppressed the production and gene expression of MUC5AC mucins, induced by PMA through the inhibition of degradation of inhibitory kappa Bα (IκBα), and NF-κB p65 nuclear translocation. Also, kaempferol inhibited EGF-induced gene expression and production of MUC5AC mucin through regulating the phosphorylation of EGFR, phosphorylation of p38 MAPK and extracellular signal-regulated kinase (ERK) 1/2 (p44/42), and the nuclear expression of specificity protein-1 (Sp1). These results suggest kaempferol regulates the gene expression and production of mucin through regulation of NF-κB and MAPK signaling pathways, in human airway epithelial cells.

• Biomolecules & Therapeutics
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• v.29 no.6
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• pp.637-642
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• 2021

In this study, we investigated whether eriodictyol exerts an effect on the production and gene expression of MUC5AC mucin in human pulmonary epithelial NCI-H292 cells. The cells were pretreated with eriodictyol for 30 min and then stimulated with phorbol 12-myristate 13-acetate (PMA) for 24 h. The effect of eriodictyol on PMA-induced nuclear factor kappa B (NF-κB) signaling pathway was also investigated. Eriodictyol suppressed the MUC5AC mucin production and gene expression induced by PMA via suppression of inhibitory kappa Bα degradation and NF-κB p65 nuclear translocation. These results suggest that eriodictyol inhibits mucin gene expression and production in human airway epithelial cells via regulation of the NF-κB signaling pathway.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.1
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• pp.127-131
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• 2013

Trastuzumab is the first molecular targeting drug to increase the overall survival rate in advanced gastric cancer. However, it has also been found that a high intrinsic or primary trastuzumab resistance exists in some proportion of gastric cancer patients. In order to explore the mechanism of resistance to trastuzumab, firstly we investigated the expression of MUC1 (membrane-type mucin 1) in gastric cancer cells and its relationship with drug-resistance. Then using gene-silencing, we transfected a siRNA of MUC1 into drug-resistant cells. The results showed the MKN45 gastric cell line to be resistant to trastuzumab, mRNA and protein expression of MUC1 being significantly upregulated. After transfection of MUC1 siRNA, protein expression of MUC1 in MKN45cells was significantly reduced. Compared with the junk transfection and blank control groups, the sensitivity to trastuzumab under MUC1 siRNA conditions was significantly increased. These results imply that HER2-positive gastric cancer cell MKN45 is resistant to trastuzumab and this resistance can be cancelled by silencing expression of the MUC1 gene.

• Biomolecules & Therapeutics
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• v.30 no.5
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• pp.473-478
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• 2022

In this study, we examined whether engeletin exerts an effect on the gene expression of MUC5AC mucin, in human pulmonary epithelial NCI-H292 cells. The cells were pretreated with engeletin for 30 min and stimulated with phorbol 12-myristate 13-acetate (PMA), for the following 24 h. The effect of engeletin on PMA-induced nuclear factor kappa B (NF-kB) signaling pathway was also investigated. Engeletin suppressed the mRNA expression and production of MUC5AC mucin, induced by PMA through the inhibition of degradation of inhibitory kappa Bα (IkBα) and NF-kB p65 nuclear translocation. These results suggest engeletin inhibits the gene expression of mucin through regulation of NF-kB signaling pathway, in human airway epithelial cells.

• Biomolecules & Therapeutics
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• v.31 no.5
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• pp.544-549
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• 2023

In this study, artesunate, an antimalarial agent, was investigated for its potential effect on the gene expression of airway MUC5AC mucin. The human pulmonary epithelial NCI-H292 cells were pretreated with artesunate for 30 min and then stimulated with phorbol 12-myristate 13-acetate (PMA), for the following 24 h. The effect of artesunate on PMA-induced nuclear factor kappa B (NF-kB) signaling pathway was also examined. Artesunate inhibited the glycoprotein production and mRNA expression of MUC5AC mucins, induced by PMA through the inhibition of degradation of inhibitory kappa Bα (IkBα) and NF-kB p65 nuclear translocation. These results suggest artesunate suppresses the gene expression of mucin through regulation of NF-kB signaling pathway, in human pulmonary epithelial cells.