• Tuberculosis and Respiratory Diseases
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• v.70 no.3
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• pp.206-217
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• 2011

Background: Transcription factor FOXP3 characterizes the thymically derived regulatory T cells. FOXP3 is expressed by cancer cell itself and FOXP3 expression was induced by TGF-${\beta}$ treatment in pancreatic cancer cell line. However, the expression of FOXP3 expression is not well known in patients with lung cancer. This study was conducted to investigate the expression of FOXP3 in patients with lung cancer and to investigate the regulation of FOXP3 expression by the treatment of TGF-${\beta}$ and DNA methyltransferase inhibitor in lung cancer cell lines. Methods: FOXP3 expression in the tissue of patients with resected non-small cell lung cancer (NSCLC) was evaluated by immunohistochemistry. The regulation of FOXP3 expression was investigated by Western blot and RT-PCR after lung cancer cell lines were stimulated with TGF-${\beta}1$ and TGF-${\beta}2$. The regulation of FOXP3 expression was also investigated by RT-PCR and flow cytometry after lung cancer cell lines were treated with DNA methyltransferase inhibitor (5-AZA-dC). Results: FOXP3 expression was confirmed in 27% of patients with NSCLC. In NCI-H460 cell line, TGF-${\beta}2$ decreased FOXP3 mRNA and protein expressions. In A549 cell line, both TGF-${\beta}1$ and TGF-${\beta}2$ decreased FOXP3 mRNA and protein expressions. 5-AZA-dC increased FOXP3 mRNA expression in NCI-H460 and A549 cell lines. Moreover, 5-AZA-dC increased intracellular FOXP3 protein expression in A549 cell lines. Conclusion: It was shown that FOXP3 is expressed by cancer cell itself in patients with NSCLC. Treatment of TGF-${\beta}2$ and DNA methyltransferase inhibitor seems to be associated with the regulation of FOXP3 expression in lung cancer cell lines.

• Journal of the Korean Society of Food Science and Nutrition
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• v.31 no.4
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• pp.691-695
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• 2002

This study was performed to examine the cytotoxic effects of the distilled pine-needle extracts against several cancer cell lines. First, cell lines including mice leukemic cancer cell line (L1210), sarcoma 180 and human monocyte-like cancer cells (U937) were tested using XTT methods in uitro. Pine-needle extracts were prepared by pressing the pine needles and distilling it at below 98$^{\circ}C$ and then added to the growth medium in a final dilution of 10, 20, and 40 times. Growth of three kinds of cancer cells was significantly inhibited by more than 50% with the addition of the extracts. Fifty six to seventy six % of inhibition was shown with the 40 times dilution of the extracts. Greater inhibition was achieved with the 20 times dilution (81~90%) and the 10 times dilution (77~89%) of the extracts. Next, other human cancer cell lines including 3 kinds of breast cancer cell lines (T47D, MDA-MB-231 and MW7A) and one hepatoma cell line (SNU-354) were tested with the 20 times dilution of the extract. T47D and MDA-MB-231 cell lines showed lower inhibition (12%) with the addition of the extract. However, MH7A and SNU-354 cell lines showed 64% and 72% inhibition with the extract, respectively. These results suggest that the distilled pine-needle extracts have strong cytotoxic effect on certain cancer cell lines and the intensity of the effect may vary depending on the process of the pine needle.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.2
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• pp.685-689
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• 2013

Objective: To study the effects of down-regulation of HDAC6 expression on proliferation, cell cycling and migration of esophageal squamous cell carcinoma (ESCC) cells and related molecular mechanisms. Methods: ESCC cell line EC9706 cells were randomly divided into untreated (with no transfection), control siRNA (transfected with control siRNA) and HDAC6 siRNA (transfected with HDAC6 small interfering RNA) groups. Effects of HDAC6 siRNA interference on expression of HDAC6 mRNA and protein in EC9706 cells were investigated by semi-quantitative RT-PCR, Western blotting and immunocytochemistry methods. Effects of down-regulation of HDAC6 expression on cell proliferation, cell cycle, and cell migration were studied using a CCK-8 kit, flow cytometry and Boyden chambers, respectively. Changes of mRNA and protein expression levels of cell cycle related factor (p21) and cell migration related factor (E-cadherin) were investigated by semi-quantitative RT-PCR and Western blotting methods. Results: After transfection of HDAC6 siRNA, the expression of HDAC6 mRNA and protein in EC9706 cells was significantly downregulated. In the HDAC6 siRNA group, cell proliferation was markedly inhibited, the percentage of cells in G0/G1 phase evidently increased and the percentage of cells in S phase decreased, and the number of migrating cells significantly and obviously decreased. The mRNA and protein expression levels of p21 and E-cadherin in the HDAC6 siRNA group were significantly higher than those in the untreated group and the control siRNA group, respectively. Conclusions: HDAC6 siRNA can effectively downregulate the expression of HDAC6 mRNA and protein in EC9706 cells. Down-regulation of HDAC6 expression can obviously inhibit cell proliferation, arrest cell cycling in the G0/G1 phase and reduce cell migration. The latter two functions may be closely related with the elevation of mRNA and protein expression of p21 and E-cadherin.

• Korean Journal of Head & Neck Oncology
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• v.31 no.1
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• pp.22-26
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• 2015

Small cell carcinoma of larynx has been reported as a rare disease occurring in 0.5% of larynx cancer. This tumor is known as one of the most lethal of all malignancies and associated with early recurrence and distant metastasis, leading into death. We experienced a case of a 70-year old male patient, who had admitted for sore throat and dysphagia and diagnosed as small cell carcinoma of larynx. We present small cell carcinoma of larynx with a brief review of literature.

• Korean Journal of Bronchoesophagology
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• v.7 no.1
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• pp.24-28
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• 2001

Background and Objectives： Heat shock protein(HSP) 27 is a member of the small HSP family that plays a part in the epithelial cell growth and differentiation, wound healing. apoptosis and cell protection against inflammatory cytotoxic mediators. The expression of HSP27 was investigated in normal laryngeal tissue and squamous cell carcinoma of the larynx. Materials and Methods : We studied expression of HSP27 by Western blot on 20 patients of laryngeal squamous cell carcinoma. Results： HSP27 expressed in all normal and cancer tissues. In 9 cases(45%), expression of HSP27 more prominent in cancer tissue. Statistically, there were no significant difference in the expression of HSP27 in normal and cancer tissue, clinical stage and tumor differentiation. Conclusion 45% of cancer tissues was more prominent than normal tissue. But further studies on expression of HSP27 in laryngeal cancer and relationship with clinical parameter should be done.

• BMB Reports
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• v.44 no.8
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• pp.523-528
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• 2011

To identify novel genes that are regulated by promoter methylation, a combinational approach involving in silico mining followed by molecular assay was performed. From the expression microarray data registered in the European bioinformatics institute (EBI), genes showing downregulation in breast cancer cells were initially screened and then selected by e-Northern analysis using the Unigene database. A series of these in silico methods identified CAMK2B and ARFGEF1 as candidates, and the two genes were revealed to be hypermethylated in breast cancer cell lines and hypomethylated in normal breast cell lines. Additionally, cancer cell lines showed downregulated expression of these genes. Furthermore, treatment of the cancer cell lines with a demethylation agent, 5-Aza-2'-deoxycytidine, recovered expression of CAMK2B and ARFGEF1, implying that hypermethyaltion silenced gene activity in cancer cells. Taken together, promoter methylations of CAMK2B and ARFGEF1 are novel epigenetic markers identified in breast cancer cell lines and can be utilized for the application to clinical cancer tissues.

• Biomedical Science Letters
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• v.27 no.3
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• pp.134-141
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• 2021

c-Jun N-terminal kinases (JNKs) have a Janus face, regulating both cell apoptosis and survival. The present study focused on understanding the function of JNK in tumor development and the chemoresistance underlying JNK-mediated cancer cell survival. We identified an inhibitor of JNK1, an important regulator of cancer cell survival. Kinase assay data showed that JNK1-dependent c-Jun phosphorylation was inhibited by indirubin derivatives. In particular, indirubin-3-monoxime (I3M) directly inhibited the phosphorylation of c-Jun in vitro, with a half inhibition dose (IC₅₀) of 10 nM. I3M had a significant inhibitory effect on JNK1 activity. Furthermore, we carried out assays to determine the viability, migration, and proliferation of breast cancer cells. Our results demonstrated that cell growth, scratched wound healing, and colony forming abilities were inhibited by the JNK inhibitor SP600125 and I3M. The combination of SP600125 and I3M significantly decreased cancer cell proliferation, compared with either SP600125 or I3M alone. Our studies may provide further support for JNK1-targeting cancer therapy using the indirubin derivative I3M in breast cancer.

• Journal of Applied Biological Chemistry
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• v.63 no.4
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• pp.457-462
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• 2020

Pancreatic cancer is among the most difficult-to-treat tumors. More than half of patients with this cancer have very few symptoms at the early stages, allowing the development of distant metastases and resistance to cancer treatment. In this study, we found that Juniperus chinensis extract (JCX) decreased the cell viability and migration activity of PANC-1 and SNU-213 pancreatic cancer cells in a dose-dependent manner. JCX increased caspase-3 activation and generation of reactive oxygen species (ROS). N-acetylcysteine treatment blocked JCX-induced ROS generation and the negative effects on pancreatic cancer cell viability. In addition, JCX down-regulated the levels of phospho-focal adhesion kinase (p-FAK) and phospho-extracellular signal-regulated kinase (p-ERK). Together, these results indicate that JCX induces apoptosis in human pancreatic cancer cell lines through ROS production, downregulating FAK/ERK signaling and activating caspase-3. We propose that JCX-derived compounds represent candidates for the development of alternative medicines for the treatment of pancreatic cancer.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.8
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• pp.4037-4043
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• 2012

Despite progress in elucidating mechanisms associated with colorectal cancer and improvement of treatment methods, it remains a frequent cause of death worldwide. New and more effective therapies are therefore urgently needed. Recent studies have shown that immunogenicity of whole ovarian tumor cells and subsequent T cell response were potentiated by oxidation modification with hypochlorous acid (HOCl) in vitro and ex vivo. These results prompted us to investigate the protective antitumor response with an HOCl treated CT26 colorectal cancer cell vaccine in an in vivo mouse model. Administration of HOCl modified vaccine triggered robust antitumor immunity to autologous tumor cells in mice and prolonged survival period significantly. In addition, increased necrosis and apoptosis were found in tumor tissue from the oxidation group. Interestingly, ELISPOT assays showed that specific T cell responses were not elicited in response to the immunizing cellular antigen, in contrast to raising sera antibody titer and antibody binding activity shown by ELISA assay and flow cytometry. Further evaluation of the mechanisms underlying HOCl modified vaccine mediated humoral immunity highlighted the role of antibody-dependent cell-mediated cytotoxicity. These results combined with previous studies suggest that HOCl oxidation modified whole cell vaccine has wide applicability as a cancer vaccine because it can target both T cell- and B cell-specific responses. It may thus represent a promising approach for the immunotherapy of colorectal cancer.

• Korean Journal of Pharmacognosy
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• v.25 no.4 s.99
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• pp.382-387
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• 1994

Antineoplastic activity against human gastric and colon carcinoma cell lines was measured in 49 extracts from 46 plants using MTT (3-[4, 5-dimethyl thiazol-2-yl]-2, 5-diphenyl tetrazolium bromide) method. Six extracts from five plants have been reported to have antineoplastic effect. Extracts from remaining 41 plants failed to show significant cytotoxic effect at the concentration of less than $230\;{\mu}g/ml$.