• Asian Pacific Journal of Cancer Prevention
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• v.13 no.11
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• pp.5557-5562
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• 2012

Aim: The aim of this study was to investigate the frequency and correlation between auto-antibodies to survivin and MUC1 variable number tandem repeats (VNTR) in colorectal cancer (CRC), which can provide valuable information for the design of immunotherapeutic vaccines for this disease. Methods: Enzyme-linked immunosorbent assays (ELISA) were used to examine the level of auto-antibodies against survivin and MUC1 VNTR in the serum of 135 CRC patients and 95 healthy volunteers. Results: Using mean absorbance + 2 standard deviations (SD) of the healthy samples as a cut-off value, the positive rates of survivin and MUC1 VNTR auto-antibodies in CRC were 31.1% and 18.5%, respectively. Altogether, the survivin and MUC1 VNTR positive samples accounted for 36.3% of the CRC patients, and 7.4% were positive for both. Conclusion: A significant positive correlation was found between levels of specific antibodies against survivin and MUC1 VNTR in the serum of CRC patients (r = 0.3652, P < 0.0001), suggesting that vaccines against both targets would elicit immune responses more effectively.

• The Journal of Internal Korean Medicine
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• v.29 no.3
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• pp.765-777
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• 2008

Objectives : In this study, the author tried to examine whether Gamijinhae-tang and Socheongryong-tang-ga-seokgo significantly affect both PMA-induced mucin production and MUC5AC gene expression from airway epithelial cells. Materials and Methods : Confluent NCI-H292 cells were pretreated for 30 min in the presence of JHT and STS and treated with PMA (10ng/ml), to assess the effects of the agents on PMA-induced mucin production by enzyme-linked immunosorbent assay (ELISA). Also, the effects of the agents on PMA-induced MUC5AC gene expression from the same cells were investigated. Possible cytotoxicities of the agent were assessed by examining the rate of survival and proliferation of NCI-H292 cells after treatment of agents during 48 hrs. Results : (1) JHT and STS did not show significant cytotoxicity to NCI-H292 cells. (2) JHT significantly decreased PMA-induced mucin production from NCI-H292 cells. However. STS did not affect mucin production. (3) JHT significantly inhibit the expression levels of PMA-induced MUC5AC gene in NCI-H292 cells. STS slightly decreased the expression levels of PMA-induced MUC5AC gene. Conclusion : These results suggest that JHT can not only affect the production of mucin but also affect the expression of the mucin gene, and this explains the traditional use of JHT in oriental medicine. The effects of JHT and STS with their components should be further investigated using animal experimental models that simulate pathophysiology of airway diseases through future studies.

• Biomolecules & Therapeutics
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• v.30 no.6
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• pp.540-545
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• 2022

Betulin is a triterpenoid natural product contained in several medicinal plants including Betulae Cortex. These medicinal plants have been used for controlling diverse inflammatory diseases in folk medicine and betulin showed anti-inflammatory, antioxidative, and anticancer activities. In this study, we tried to examine whether betulin exerts a regulative effect on the gene expression of MUC5AC mucin under the status simulating a pulmonary inflammation, in human airway epithelial cells. Confluent NCI-H292 cells were pretreated with betulin for 30 min and then stimulated with phorbol 12-myristate 13-acetate (PMA) for 24 h or the indicated periods. The MUC5AC mucin mRNA expression and mucin glycoprotein production were measured by reverse transcription - polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. To elucidate the action mechanism of betulin, effect of betulin on PMA-induced nuclear factor kappa B (NF-kB) signaling pathway was also investigated by western blot analysis. The results were as follows: 1) Betulin significantly suppressed the production of MUC5AC mucin glycoprotein and down-regulated MUC5AC mRNA expression induced by PMA in NCI-H292 cells. 2) Betulin inhibited NF-κB activation stimulated by PMA. Suppression of inhibitory kappa B kinase (IKK) by betulin led to the inhibition of the phosphorylation and degradation of inhibitory kappa B alpha (IκBα), and the nuclear translocation of NF-κB p65. This, in turn, led to the down-regulation of MUC5AC glycoprotein production in NCI-H292 cells. These results suggest betulin inhibits the gene expression of mucin through regulation of NF-kB signaling pathway, in human airway epithelial cells.

• The Journal of Internal Korean Medicine
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• v.30 no.4
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• pp.685-695
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• 2009

Objectives : In this study, the author tried to investigate whether Geonpye-tang(GPT) significantly affects PMA-, EGF- or TNF-alpha-induced MUC5AC mucin production and gene expression from human airway epithelial cells. Materials and Methods : Effects of the agent on PMA-, EGF- or TNF-alpha-induced MUC5AC mucin production and gene expression from human airway epithelial cells (NCI-H292) were investigated. Confluent NCI-H292 cells were pretreated for 30 min in the presence of GPT and treated with PMA (10ng/ml) or EGF (25ng/ml) or TNF-alpha (0.2nM), to assess both effect of the agent on PMA- or EGF- or TNF-alpha-induced MUC5AC mucin production by enzyme-linked immunosorbent assay (ELISA) and gene expression by reverse transcription-polymerase chain reaction (RT-PCR). Possible cytotoxicity of the agent was assessed by examining the rate of survival and proliferation of NCI-H292 cells after treatment with the agent over 72 hrs (SRB assay). Results : (1) GPT significantly inhibited PMA-induced and EGF-induced MUC5AC mucin production from NCI-H292 cells. However, GPT did not affect TNF-alpha-induced MUC5AC mucin production. (2) GPT significantly inhibited the expression levels of PMA-, EGF- or TNF-alpha-induced MUC5AC genes in NCI-H292 cells (3) GPT did not show significant cytotoxicity to NCI-H292 cells. Conclusion : This result suggests that GPT can affect the production and gene expression of respiratory mucin observed in diverse respiratory diseases accompanied by mucus hypersecretion. This can explain the traditional use of GPT in oriental medicine. Effects of GPT with their components should be further investigated using animal experimental models that reflect pathophysiology of airway diseases through future studies.

• Biomolecules & Therapeutics
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• v.18 no.4
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• pp.396-401
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• 2010

We conducted this study to investigate whether baicalin, baicalein or schizandrin significantly affect MUC5AC mucin production induced by epidermal growth factor (EGF) or phorbol ester (PMA) in human airway epithelial cells. Confluent NCI-H292 cells were pretreated with varying concentrations of baicalin, baicalein or schizandrin for 30 min and then stimulated with EGF or PMA for 24 h, respectively. MUC5AC mucin protein production was measured by ELISA. The results were as follows: (1) Baicalin was found to inhibit the production of MUC5AC mucin protein induced by both EGF and PMA. (2) Baicalein, the aglycone of baicalin, also inhibited MUC5AC mucin production. (3) Schizandrin, derived from Schizandrae Fructus, inhibited MUC5AC mucin production by the same inducers. These results suggest that baicalin, baicalein and schizandrin can regulate the production of mucin protein by directly acting on human airway epithelial cells.

• Tuberculosis and Respiratory Diseases
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• v.70 no.3
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• pp.218-223
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• 2011

Background: We investigated whether curcumin and genistein affect the MUC5AC mucin production from human airway epithelial cells that is induced by phorbol 12-myristate 13-acetate (PMA) or tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$). Methods: Confluent NCI-H292 cells were pretreated with each agent for 30 min and then stimulated with PMA or TNF-${\alpha}$ for 24 hours. MUC5AC mucin production was measured by an ELISA. Results: (1) Curcumin dose-dependently inhibited the production of MUC5AC mucin that was induced by PMA or TNF-${\alpha}$; (2) Genistein inhibited PMA-induced MUC5AC mucin production. However, it did not decrease TNF-${\alpha}$-induced MUC5AC mucin production. Conclusion: These results suggest that curcumin and genistein inhibit the production of airway mucin induced by PMA.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.15
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• pp.6269-6273
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• 2014

Growing evidence suggests that miR-150-5p has an important role in regulating genesis of various types of cancer. However, the roles and the underlying mechanisms of miR-150-5p in development of colorectal cancer (CRC) remain largely unknown. Transwell chambers were used to analyze effects on cell migration and invasion by miR-150-5p. Quantitative real-time PCR (qRT-PCR), Western blotting and dual-luciferase 3' UTR reporter assay were carried out to identify the target genes of miR-150-5p. In our research, miR-150-5p suppressed CRC cell migration and invasion, and MUC4 was identified as a direct target gene. Its effects were partly blocked by re-expression of MUC4. In conclusiomn, miR-150-5p may suppress CRC metastasis through directly targeting MUC4, highlighting its potential as a novel agent for the treatment of CRC metastasis.

• 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.

• Journal of Microbiology and Biotechnology
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• v.25 no.10
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• pp.1751-1760
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• 2015

Mucin2 (MUC2), an important regulatory factor in the immune system, plays an important role in the host defense system against bacterial translocation. Probiotics known to regulate MUC2 gene expression have been widely studied, but the interactions among probiotic, pathogens, and mucin gene are still not fully understood. The aim of this study was to investigate the role of MUC2 in blocking effects of probiotics on meningitic E. coli-induced pathogenicities. In this study, live combined probiotic tablets containing living Bifidobacterium, Lactobacillus bulgaricus, and Streptococcus thermophilus were used. MUC2 expression was knocked down in Caco-2 cells by RNA interference. 5-Aza-2'-deoxycytidine (5-Aza-CdR), which enhances mucin-promoted probiotic effects through inducing production of Sadenosyl-L-methionine (SAMe), was used to up-regulate MUC2 expression in Caco-2 cells. The adhesion to and invasion of meningitic E. coli were detected by competition assays. Our studies showed that probiotic agents could block E. coli-caused intestinal colonization, bacteremia, and meningitis in a neonatal sepsis and meningitis rat model. MUC2 gene expression in the neonatal rats given probiotic agents was obviously higher than that of the infected and uninfected control groups without probiotic treatment. The prohibitive effects of probiotic agents on MUC2-knockdown Caco-2 cells infected with E44 were significantly reduced compared with nontransfected Caco-2 cells. Moreover, the results also showed that 5-Aza-CdR, a drug enhancing the production of SAMe that is a protective agent of probiotics, was able to significantly suppress adhesion and invasion of E44 to Caco-2 cells by upregulation of MUC2 expression. Taken together, our data suggest that probiotic agents can efficiently block meningitic E. coli-induced pathogenicities in a manner dependent on MUC2.