• Mycobiology
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• v.51 no.2
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• pp.94-108
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• 2023

Termitomyces sp. that grow in symbiosis with fungus-farming Termites have medicinal properties. However, they are rare in nature, and their artificial culture is challenging. The expression of AXL receptor tyrosine kinase and immune checkpoint molecules favor the growth of cancer cells. The study evaluated the optimal conditions for the artificial culture of Termitomyces and their inhibitory activity on AXL and immune checkpoint molecules in lung adenocarcinoma and melanoma cell lines. The culture of 45 strains of Termitomyces was compared. Five strains with marked growth rates were selected. Four of the selected strains form a single cluster by sequence analysis. The mycelium of 4 selected strains produces more fungal mass in potato dextrose broth than in a mixed media. The bark was the most appropriate solid substrate for Termitomyces mycelia culture. The mycelium of all five selected strains showed a higher growth rate under normal CO₂ conditions. The culture broth, methanol, and ethyl acetate of one selected strain (T-120) inhibited the mRNA relative expression of AXL receptor tyrosine kinase and immune checkpoint molecules in cancer cell lines. Overall, these results suggest the potential usefulness of Termitomyces extracts as a coadjuvant therapy in malignant diseases.

• Korean Journal of Veterinary Research
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• v.32 no.1
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• pp.77-82
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• 1992

A noncytopathic bovine viral diarrhea virus(NC BVDV) strain isolated and purified from persistently infected primary bovine fetal lung(BFL) cells was studied by biophysical methods. The buoyant density of particles of the NC BVDV strain was shown to be between 1,090 and $1,114g/cm^3$ and the maximum virus infectivity occured at $1,098g/cm^3$. Immunoelectron microscopic examination by using the partially purified virus revealed regular spherical particles 30~80nm in diameter. Differences in the genomic size of cytopathic and noncytopathic BVDV from infected cells were not found. A comparison of viral proteins of a noncytopathic and cytopathic strain(NADL) by immunoprecipitation using monoclonal antibody indicated that NC BVDV, compared to cytopathic NADL, was cell associated.

• Tuberculosis and Respiratory Diseases
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• v.80 no.3
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• pp.247-254
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• 2017

Background: Airway epithelial cells are the first line of defense, against pathogens and environmental pollutants, in the lungs. Cellular stress by cadmium (Cd), resulting in airway inflammation, is assumed to be directly involved in tissue injury, linked to the development of lung cancer, and chronic obstructive pulmonary disease (COPD). We had earlier shown that ACN9 (chromosome 7q21), is a potential candidate gene for COPD, and identified significant interaction with smoking, based on genetic studies. However, the role of ACN9 in the inflammatory response, in the airway cells, has not yet been reported. Methods: We first checked the anatomical distribution of ACN9 in lung tissues, using mRNA in situ hybridization, and immunohistochemistry. Gene expression profiling in bronchial epithelial cells (BEAS-2B), was performed, after silencing ACN9. We further tested the roles of ACN9, in the intracellular mechanism, leading to Cd-induced production, of proinflammatory cytokines in BEAS-2B. Results: ACN9 was localized in lymphoid, and epithelial cells, of human lung tissues. ACN9 silencing, led to differential expression of 216 genes. Pathways of sensory perception to chemical stimuli, and cell surface receptor-linked signal transduction, were significantly enriched. ACN9 silencing, further increased the expression of proinflammatory cytokines, in BEAS-2B after Cd exposure. Conclusion: Our findings suggest, that ACN9 may have a role, in the inflammatory response in the airway.

• The Journal of Korean Medicine
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• v.31 no.3
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• pp.34-46
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• 2010

Objective: This experimental study was performed to examine if Hang-Am-Dan non-boiled water extracts (HAD-N) induce apoptosis in human lung carcinoma NCI-H460 cells in vitro and inhibits the growth of NCI-H460 cell-transplanted solid tumor in vivo. Materials and Methods: We cultured NCI-H460 cell lines and xenografted them to nude mice. The mice were divided into 3 groups, NCI-H460 cell alone, NCI-H460 + 90 mg/kg HAD-N treated group, and NCI-H460 + 180 mg/kg HAD-N treated group, with seven mice per group. HAD-N was orally administrated every day for four weeks. We checked their body weight and tumor weight and volumes two times a week and their absolute organ weight and biochemical blood analysis at the final day by sacrificing them. We also calculated their tumor inhibition rate (IR), mean survival time and percent increase in life span (% ILS). Results: In this study, we observed that all of the HAD-N treated mice got smaller tumors. The more doses of HAD-N used, the less IR showed at the 8th day after starting this experiment. Tumor weight and volume of HAD-N treatment groups also decreased. Mean survival time and percent increase in life span (% ILS) in the high-dose HAD-N treatment groups were higher than those of other groups. The test substances in the blood level UN results showed reduction in the significance in both HAD-N 90 mg/kg and HAD-N 180 mg/kg (p<0.01). The blood level phosphatase results in HAD-N 90 mg/kg group compared to NCI-H460 cell alone group showed a reduction in significance (p<0.05). AST levels HAD-N 180 mg/kg group compared to NCI-H460 cell alone group significance as well (p<0.05). Conclusion: We suggest that the results of the in vivo study showed that HAD-N may have potential as a growth inhibitor of tumor-induced NCI-H460 of nude mice in spite of the shortcomings of this study. More studies to overcome those shortcomings and to find out significant antitumor mechanism will be needed.

• Tuberculosis and Respiratory Diseases
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• v.76 no.3
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• pp.114-119
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• 2014

Background: Epigallocatechin-3-gallate (EGCG), a major biologically active component of green tea, has anti-cancer activity in human and animal models. We investigated the schedule-dependent effect of EGCG and paclitaxel on growth of NCI-H460 non-small cell lung cancer cells. Methods: To investigate the combined effect of EGCG (E) and paclitaxel (P), combination indices (CIs) were calculated, and cell cycle analysis was performed. For the effect on cell apoptosis, western blot analysis was also performed. Results: CI analysis demonstrated that both concurrent and sequential E ${\rightarrow}$ P treatments had antagonistic effects (CIs >1.0), but sequential P ${\rightarrow}$ E had synergistic effects (CIs <1.0), on the growth inhibition of NCI-H460 cells. In the cell cycle analysis, although paclitaxel induced $G_2/M$ cell cycle arrest and increased the sub-G1 fraction, concurrent EGCG and paclitaxel treatments did not have any additive or synergistic effects compared with the paclitaxel treatment alone. However, western blot analysis demonstrated that sequential P ${\rightarrow}$ E treatment decreased the expression of Bcl-2 and procaspase-3 and increased poly(ADP-ribose) polymerase (PARP) cleavage; while minimal effects were seen with concurrent or sequential E ${\rightarrow}$ P treatments. Conclusion: Concurrent or sequential E ${\rightarrow}$ P treatment had opposite effects to P ${\rightarrow}$ E treatment, where P ${\rightarrow}$ E treatment showed a synergistic effect on growth inhibition of NCI-H460 cells by inducing apoptosis. Thus, the efficacy of EGCG and paclitaxel combination treatment seems to be schedule-dependent.

• Tuberculosis and Respiratory Diseases
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• v.50 no.5
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• pp.549-556
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• 2001

Background : IGF-I is an important mitogen in many types of malignancies. Tumors also express many IGF binding proteins, which modulate IGF action. The propose of this study was to evaluate the effect of IGF-I and IGFBP on cell proliferation in mouse lung cancer cells (3LL). Methods : The cellular proliferation of 3LL with the treatment of growth factors was evaluated using MTT assay. Western ligand blot was performed in order to determine whether 3LL cells secrete IGFBPs and we evaluated the effect of IGFBP on cellular proliferation. Results : The treatment of 3LL cells with IGF-I increased cellular proliferation in a serum free media. Western ligand blot of conditioned medium of 3LL with $^{125}I$-IGF-I demonstrated one single major band with an estimated molecular mass of 24 kDa. This band was identified as IGFBP-4 with immunoblot analysis using antisera. The addition of anti-IGFBP-4 antibody to abrogate the effect of IGFBP-4 resulted in increased cellular proliferation suggesting that IGFBP-4 inhibits cell growth. Conclusion : IGF-I increases cellular proliferation, however the secreted IGFBP-4 has an inhibitory function on cell growth in 3LL. These findings suggest that IGF-I and IGFBP are involved in the cell proliferation.

• Journal of Life Science
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• v.21 no.2
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• pp.286-291
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• 2011

Hypoxia is a common condition found in a wide range of solid tumors and is often associated with metastasis and poor clinical outcomes. In the present study, we found that HIF-$1{\alpha}$ was induced by cobalt chloride (500 ${\mu}M$) treatment on human lung cancer cells, A549 and H460, for 24 hr. However, cobalt chloride (500 ${\mu}M$) did not affect cell proliferation of A549 and H460 in 48 hr. Cobalt chloride (500 ${\mu}M$) additionally induced epithelial-to-mesenchymal-like transition (EMT) such as reduced E-cadherin expression and increased ${\alpha}$-SMA expression. These results were confirmed by immunofluorecence experiment in H460 cells. E-cadherin was localized on the outer cell membrane. However, when the cells were treated with 500 ${\mu}M$ cobalt chloride for 24 hr, diffuse E-cadherin staining was observed, characteristic of a migratory mesenchymal phenotype. We also found that cobalt chloride induced integrin ${\beta}3$ expression and FAK phosphorylation in human lung cancer cells using western blotting and FACS anlaysis. Our data suggest that integrin ${\beta}3$-induced FAK phosphorylation may be developed into target molecules for blocking tumor metastasis.

• Tuberculosis and Respiratory Diseases
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• v.51 no.3
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• pp.201-210
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• 2001

Background : Approximately 10-13% of patients with interstitial lung disease(ILD) die of lung cancer, and patients with ILD have been reported to have a 7 fold higher incidence of lung cancer compared to the normal population. Recently, overexpression of the p53 and p21 proteins were observed in the epithelial cells from pathologic specimens of ILD. Overexpression of these proteins may result from chronic or recurrent DNA damage by unknown causes of inflammation. However, these proteins may also contribute to oncogenesis if other genetic alterations such as K-ras are superimposed. Methods : Immunohistochemical stains for p53 and K-ras proteins were performed with pathologic specimens from 38 cases with ILD(M/F : 27/11, mean agea : $54{\pm}10$ years) and from 10 control subjects. Results : The p53 protein was expressed in 21.1% (8/38 ILD cases) and K-ras protein expression was observed in 65.8% (25/38 ILD cases). However, neither p53 nor the K-ras protein staining was observed in the control subjects. Conclusion : A significant proportion of cases with ILD expressed the p53 and K-ras proteins in their bronchial epithelial cells. These proteins may be potentially oncogenic with the addition of further genetic alterations. However, to clarify the significance of these findings, further studies looking for correlations with the incidence of lung cancer and other genetic changes are needed.

• Journal of Chest Surgery
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• v.29 no.9
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• pp.1031-1035
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• 1996

International Ass ciation for the Study of Lung Cancer(IASLC) recommended the following classification of small cell lung carcinoma(SCLC) : (1) Small cell carcinoma (2) Mixed small cell/large cell carcinoma (3) Combined small cell carcinoma. Combined small cell carcinomas contain a squamous cell carcinoma or adenocarcinoma component. The prognostic significance of these elements is not known, but since the frequency and extent of non-small cell elements are considerably greater in posttherapy and autopsy tissues, it is possible that the non-SCLC elements are more resistant to therapy than the SCLC cells. Metaplasia & dysplasia of the bronchial surface epithelium are frequently observed in the bronchial biopsy specimens that contain small cell carcinoma of the lung. We report a case of combined small cell carcinoma with squamous element associated with microinvasive squamous cell carcinoma of the bronchial surface epithelium in 68 year old male patient, stage was IIIa. The two lesion are not connected n serial sections.

• Journal of Chest Surgery
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• v.32 no.10
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• pp.910-915
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• 1999

Background: Positron emission tomography(PEFT) using fluorine-18 deoxyglucose(FDG), showing increased FDG uptake and retention in malignant cells, has been proven to be useful in differentiating malignant from benign tissues. We indertook the prospective study to compare the accuracy of the whole-body FDG PET with that of the conventional chest computed tomography(CT) for nodal staging of non-small-cell lung cancers(NSCLC). Material and Method: FDG PET and contrast enhanced CT were performed in 36 patients with potentially resectable NSCLC. Each Imaging study was evaluated independently, and nodal stations were localized according to the AJCC regional lymph nodes mapping system. Extensive lymph node dissection(1101 nodes) of ipsi- and contralateral mediastinal nodal stations was performed at thoracotomy and/or mediastinoscopy. Image findings were compared with the histopathologic staging results and were analyzed with the McNema test(p) and Kappa value(k). Result: The sensitivity, specificity, positive predictive value, and negative predictive value of CT for ipsilateral mediastinal nodal staging were 38%, 68%, 25%, 79%, and 61%, and those of PET were 88%, 71%, 47%, 95%, and 75%(p>0.05, K=0.29). When analyzed by individual nodal group(superior, aortopulmonary window, and inferior), the sensitivity, specificity, positive predictive value, and negative predictive value of CT were 27%, 82%, 22%, 85%, and 73%, and those of PET were 60%, 87%, 92%, and 82%(p<0.05, k=0.27). Conclusion: FDG PET in addition to CT appears to be superior to CT alone for mediastinal staging of non-small cell lung cancers.