• Tuberculosis and Respiratory Diseases
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• v.86 no.4
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• pp.294-303
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• 2023

Background: The human lung serves as a niche for a unique and dynamic bacterial community related to the development and aggravation of multiple respiratory diseases. Therefore, identifying the microbiome status is crucial to maintaining the microecological balance and maximizing the therapeutic effect on lung diseases. Therefore, we investigated the histological type-based differences in the lung microbiomes of patients with lung cancer. Methods: We performed 16S rRNA sequencing to evaluate the respiratory tract microbiome present in bronchoalveolar lavage fluid. Patients with non-small cell lung cancer were stratified based on two main subtypes of lung cancer: adenocarcinoma and squamous cell carcinoma (SqCC). Results: Among the 84 patients analyzed, 64 (76.2%) had adenocarcinoma, and 20 (23.8%) had SqCC. The α- and β-diversities showed significant differences between the two groups (p=0.004 for Chao1, p=0.001 for Simpson index, and p=0.011 for PERMANOVA). Actinomyces graevenitzii was dominant in the SqCC group (linear discriminant analysis [LDA] score, 2.46); the populations of Haemophilus parainfluenza (LDA score, 4.08), Neisseria subflava (LDA score, 4.07), Porphyromonas endodontalis (LDA score, 3.88), and Fusobacterium nucleatum (LDA score, 3.72) were significantly higher in the adenocarcinoma group. Conclusion: Microbiome diversity is crucial for maintaining homeostasis in the lung environment, and dysbiosis may be related to the development and prognosis of lung cancer. The mortality rate was high, and the microbiome was not diverse in SqCC. Further large-scale studies are required to investigate the role of the microbiome in the development of different lung cancer types.

• Archives of Pharmacal Research
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• v.29 no.11
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• pp.1018-1023
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• 2006

Chemoresistance remains the major obstacle to successful therapy of cancer. In order to understand the mechanism of multidrug resistance (MDR) that is frequently observed in lung cancer patients, here we studied the contribution of MDR-related proteins by establishing lung cancer cell lines with acquired resistance against etoposide. We found that human H460 lung cancer cells responded to etoposide more sensitively than A549 cells. Among MDR-related proteins, the expression of p-glycoprotein (Pgp) and lung resistance protein (LRP) were much higher in A549 cells compared with that in H460 cells. When we established H460-R1 and -R2 cell lines by progressive exposure of H460 cells to increasing doses of etoposide, the response against etopbside as well as doxorubicin was greatly reduced in R1 and R2 cells, suggesting MDR induction. Induction of MDR was not accompanied by a decrease in the intracellular accumulation of etoposide and the expression of MDR-related proteins that function as drug efflux pumps such as Pgp and MRP1 was not changed. We found that the acquired resistance paralleled an increased expression of LRP in H460 cells. Taken together, our data suggest the implicative role of LRP in mediating MDR in lung cancer.

• Biomedical Science Letters
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• v.29 no.4
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• pp.336-343
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• 2023

Lung cancer is one of the cancers with high mortality and incidence rates worldwide. Although, various anticancer research efforts are underway to completely treat cancer, the challenge against it remains in the inability to eliminate cancer stem cells (CSCs), leading to difficulties in curing the cancer and resulting in recurrence. As a result, there is a growing interest in the discovery of new biomarkers and therapeutic molecules that can simultaneously target both cancer cells and CSCs. From this point of view, we focused on fibronectin leucine rich transmembrane protein 3 (FLRT3), one of the genes known to be present in human lung cells and the discovery from our previous cancer proteomic analysis study. This study aimed to evaluate the potential of FLRT3 as a specific therapeutic biomarker for lung cancer and Lung Cancer-derived-Stem Cells (LCSC). Also, to estimate the biological function of FLRT3 in cancer and LCSC, short hairpin RNA (shRNA) was generated and showed the ability of the decreased-cell migration and cell proliferation of lung cancer through ERK signaling pathway when FLRT3 was knock-downed. In conclusion, our study is the first to report that FLRT3 has the potential as therapeutic biomarker for the treatment of lung cancer and LCSC.

• Tuberculosis and Respiratory Diseases
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• v.57 no.6
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• pp.594-598
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• 2004

Signet ring cell carcinoma of lung is an unique variant of mucin producing adenocarcinoma which is characterized by abundant intracellular mucin accumulation. Only a few cases of primary signet ring cell carcinoma of lung have been reported in the world wide literature. And we have, recently experienced one case of primary signet ring cell carcinoma of lung. A 55 years old man was evaluated for paralysis of lower extremities and was found to have lung cancer in the left upper and lower lobe with pleural, multiple spinal, bone and liver metastases. Signet ring tumor cells were revealed by cytologic examination of pleural fluids. And there were no evidence of signet ring cell carcinoma of other organs. Primary signet ring cell carcinoma of lung seems to have an aggressive behavior and therapeutic modalities could be different from those for signet ring cell carcinomas from other organs. Therefore it is important to separate primary signet ring cell adenocarcinoma of lung from metastatic tumors.

• Tuberculosis and Respiratory Diseases
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• v.48 no.3
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• pp.324-330
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• 2000

Objective : Lung cancer arises after a series of morphological changes, which take several years to progress from normal epithelium to invasive cancer. Multiple molecular changes and growth factor production have been documented in lung cancers, both small cell and non-small cell types. Insulin-like growth factors(IGFs) are important mitogenic and anabolic peptides, both in vivo and in vitro, and are thought to be significant autocrine-paracrine factors involved in normal and malignant cell proliferation. In this study, the degree of expression of IGF-1 on the immunohistochemical staining in human non-small cell lung cancer(NSCLC) cells and small cell lung cancer (SCLC) cells were investigated. Methods : Immunohistochemical staining for IGF-1 was performed in 15 cases of small cell carcinoma, 15 cases of squamous cell carcinoma, 15 cases of adenocarcinoma, and 12 cases of bronchoalveolar carcinoma. Results : The expression of IGF-1 on the immunohistochemical staining significantly increased in NSCLC cells than in SCLC cells. Conclusion : These results suggest the expression of IGF-1 in human lung cancer cells. The immunohistochemical staining of IGF-1 in lung cancer cell lines may assist in the differentiation of NSCLC and SCLC.

• Journal of Chest Surgery
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• v.35 no.12
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• pp.909-913
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• 2002

The large cell neuroendocrine carcinoma is uncommon and its diagnostic criteria was recently established as pulmonary neuroendocrine carcinoma. A 74-year-old man who was a heavy smoker without symptoms was presented with a lung mass in right lower lobe. He was diagnosed as having large cell neuroendocrine carcinoma by needle biopsy. He was treated with right lower lobe lobectomy and mediastinal lymph node dissection. We experienced one case of large cell neuroendocrine carcinoma of lung and report it with reference.

• Tuberculosis and Respiratory Diseases
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• v.44 no.4
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• pp.796-805
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• 1997

Background : It is clear that deregulation of cell cycle progression is a hallmark of neoplastic transformation and genes involved in the $G_1$/S transition of the cell cycle are especially frequent targets for mutations in human cancers, including lung cancer. p16 gene product, one of the G1 cell-cycle related proteins, that is recently identified plays an important role in the negative regulation of the the kinase activity of the cyclin dependent kinase (cdk) enzymes. Therefore p16 gene is known to be an important tumor suppressor gene and is also called MTS1 (multiple tumor suppressor 1). No more oncogenes have been reported to be frequently related to multiple different malignancies than the alterations of p16 gene. Especially when it comes to non-small cell lung cancer, there was no expression of p16 in more than 70% of cell lines examined. And also it is speculated that p16 gene could exert a key role in the development of non-small cell lung cancer. This study was designed to evaluate whether p16 gene could be used as a candidate for gene therapy of non-small cell lung cancer. Methods : After the extraction of total RNA from normal fibroblast cell line and subsequent reverse transcriptase reaction and polymerase chain reaction, the amplified p16 cDNA was subcloned into eukaryotic expression plasmid vector, pRC-CMV. The constructed pRC-CMV-p16 was transfected into the NCI-H441 NSCLC cell line using lipofectin. The changes of G1 cell-cycle related proteins were investigated with Western blot analysis and immunoprecipitation after extraction of proteins from cell lysates and tumor suppressive effect was observed by clonogenic assay. Results : (1) p16(-) NCI-H441 cell line transfected with pRC-CMV-p16 showed the formation of p16 : cdk 4 complex and decreased phosphorylated Rb protein, while control cell line did not. (2) Clonogenic assay demonstrated that the number of colony formation was markedly decreased in p16(-) NCI-H441 cell line transfected with pRC-CMV-p16 than the control cell line. Conclusion : It is confirmed that the expression of p16 protein in p16 absent NSCLC cell line with the gene transfection leads to p16 : cdk4 complex formation, subsequent decrease of phosphorylated pRb protein and ultimately tumor suppressive effects. And also it provides the foundation for the application of p16 gene as a important candidate for the gene therapy of NSCLC.

• Tuberculosis and Respiratory Diseases
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• v.45 no.5
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• pp.984-991
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• 1998

Background: The 3p deletions has been shown to be the most frequent alteration in lung cancers, strongly suggesting the presence of at least one tumor suppressor gene in this chromosomal region. However, no solid candidate for the tumor suppressor gene(s) on 3p has as yet been identified. Recent attention has focused on a candidate 3p14.2 tumor suppressor gene, FHIT, which is located in a region that is homozygously deleted in multiple tumor cell lines and disrupted by the hereditary renal cell carcinoma t(3;8) chromosomal translocation breakpoint FHIT also spans FRA3B, the most common fragile sites in the human genome. In the present study, we have analyzed expression of the FHIT gene in lung cancer cell lines. Methods: RNA from 21 lung cancer cell lines (16 NSCLC, 5 SCLC) were extracted using standard procedures. Random-primed. first strand cDNAs were synthesized from total RNA and PCR amplication of coding exons 5 to 9 was performed. The RT-PCR products were electrophoresed in 1.5% ethidium bromide-stained agarose gels. Results: 12 of 21(57%) lung cancer cell lines exhibited absent or aberrant FHIT expression [7 of 16(44%) of non-small cell lung cancer and 5 of 5(100%) of small cell lung cancer cell lines]. Conclusion: The result shows that abnormal transcription of the FHIT gene is common in human lung cancer cell lines, especially in small cell lung cancer.

• The Korean Journal of Cytopathology
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• v.5 no.2
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• pp.154-159
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• 1994

Pulmonary giant cell carcinoma is one of the most highly malignant neoplasms of the lung. Although mixed malignant glandular or squamous components may be associated with a giant cell carcinoma, it is a distinct clinical and morphologic entity. We reviewed cytologic presentations of 6 cases of pulmonary giant ceil carcinoma. Cytologically, the single most characteristic feature of giant cell carcinoma was an extremely large, bizarre cancer cell engulfing numerous leukocytes. The nuclei of these cells showed occasional prominent nucleoli, and the cytoplasm was abundant. Giant cells were also seen in other types of pulmonary carcinoma, but the slant cells of this neoplasm could be differentiated from those encountered in undifferentiated large cell carcinoma and squamous cell carcinoma by the abundant cytoplasm, the presence of markedly enlarged nuclei, prominent nucleoli, and a significant degree of phagocytosis. In conclusion, precise diagnosis and classification of lung cancer is imperative because of proved correlation between cell type and prognosis.

• Journal of Chest Surgery
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• v.27 no.2
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• pp.174-176
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• 1994

Castleman`s disease is characterized by lymph node enlargement. There are two distinct histologic subtypes, which are hyaline vascular and plasma cell type. We experienced one case of localized Castleman`s disease of plasma cell type, which located in hilum of the left lung.