• Journal of Korean Academy of Oral and Maxillofacial Radiology
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• v.26 no.2
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• pp.121-132
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• 1996

The purpose of this study was to aid in the prediction of tumor cell tolerance to radiotherapy and/or chemotherapy. For this study, cell surviving curves were obtained for human osteosarcoma MG-63 cell line using semiautomated MTT assay. 2,4, 6, 8, 10Gy were irradiated at a dose rate of 210cGy/min using /sup 60/Co Irradiator ALDORADO 8. After irradiation, MG-63 cell lines(3×10⁴ cells/ml) were exposed to bleomycin and cisplatin at concentration of 0.2, 2, 20㎍/㎖ for 1 hour respectively. The viable cells were determined for each radiation dose and/or each concentration of drug. And they were compared to control values. The obtained results were as follows : 1. There was significant difference of surviving fraction at 4, 6, 8, 10Gy on MG-63 cell line(p<0.05). 2. There was significant difference of cytotoxicity of bleomycin or cisplatin at all concentration of 0.2, 2, 20㎍/㎖ (p<0.05) on MG-63 cell line. The cytotoxicity of cisplatin was more effective than bleomycin at concentration of 20㎍/㎖ on MG-63 cell line. 3. There was significant difference of cytotoxicity of bleomycin or cisplatin at all concentration after irradiation of 2Gy on MG-63 cell line. 4. There was significant difference of cytotoxicity of bloemycin or cisplatin at concentration of 20㎍/㎖ after irradiation than that of irradiation alone(p<0.01). But there was no significant difference of cytotoxicity of bleomycin at concentration of 20㎍/㎖ after irradiation of l0Gy than that of irradiation alone.

• Biomedical Science Letters
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• v.17 no.3
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• pp.261-265
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• 2011

Parkin is a putative tumor suppressor protein and its expression is frequently reduced or absent in several types of tumors. In this study, we examined the role of Parkin in mRNA expression of monocyte chemotactic protein-1 (MCP-1) in the breast cancer cell line MCF7. Expression of MCP-1 mRNA increased after TNF-${\alpha}$ treatment. However, overexpression of Parkin induced a decrease in expression of MCP-1 mRNA in TNF-${\alpha}$-stimulated MCF7. This decrease in MCP-1 mRNA by Parkin overexpression occurred in a dose- and time-dependent manner. Using a wound scratch assay, we found that Parkin overexpression in MCF7 cells also resulted in a decrease in cell migration. These results suggest that Parkin down-regulates MCP-1 synthesis leading to decreased migration of tumor cells. We suggest that one possible mechanism by which Parkin acts as a tumor suppressor is by inhibiting migration or metastasis of cancer cells.

• Journal of the Korean Applied Science and Technology
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• v.26 no.3
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• pp.297-305
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• 2009

Melanoma is the most serious type of skin cancer as a malignant tumor of melanocytes. In this work, the syntheses of a novel series of benzaminoquinoline derivatives 1a-c and their antiproliferative activities against A375 human melanoma cell line were described. All the compounds ($IC_{50}=0.78-1.02{\mu}M$) showed superior antiproliferative activities to Sorafenib ($IC_{50}=5.58{\mu}M$) as a reference compound. These results suggested that benzaminoquinoline derivatives have potentials as a therapeutic agent for the treatment for melanoma.

• The Korean Journal of Mycology
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• v.29 no.1
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• pp.61-66
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• 2001

Entomopathogenic fungus of Cordyceps militaris is famous of its medicinal efficacies. An antitumor compound was purified from the n-hexane extract of artificially cultivated fruiting bodies of C. militaris and identified as ergosterol peroxide $(5{\alpha},\;8{\alpha}-epidioxy-24(R)-methylcholesta-6,22-dien-3{\beta}-o1,\; C_{28}H_{44}O_3)$ mainly by $^1H\;and\;^{13}C-NMR$ spectroscopic techniques. When the antitumor activity of ergosterol peroxide was measured against 3 tumor cell lines from Korean cancer patients, it showed the most strong activity against gastric cancer SNU-l cell line 3 days after treatment. The 50% inhibitory concentrations $(IC_{50})$ of ergosterol peroxide 6 days after treatment were $75.8{\mu}g/ml$ for human gastric SNU-1 tumor cell line, $39.7{\mu}g/ml$ for human colorectal SNU-C4 tumor cell line and $32.7{\mu}g/ml$ for human hepatoma SNU-354 cell line.

• BMB Reports
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• v.47 no.5
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• pp.280-285
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• 2014

Cancer cells undergo uncontrolled proliferation, and aberrant mitochondrial alterations. Tumor necrosis factor receptor-associated protein 1 (TRAP1) is a mitochondrial heat shock protein. TRAP1 mRNA is highly expressed in some cancer cell lines and tumor tissues. However, the effects of its overexpression on mitochondria are unclear. In this study, we assessed mitochondrial changes accompanying TRAP1 overexpression, in a mouse cell line, NIH/3T3. We found that overexpression of TRAP1 leads to a series of mitochondrial aberrations, including increase in basal ROS levels, and decrease in mitochondrial biogenesis, together with a decrease in peroxisome proliferator-activated receptor gamma coactivator-$1{\alpha}$ (PGC-$1{\alpha}$) mRNA levels. We also observed increased extracellular signal-regulated kinase (ERK) phosphorylation, and enhanced proliferation of TRAP1 overexpressing cells. This study suggests that overexpression of TRAP1 might be a critical link between mitochondrial disturbances and carcinogenesis.

• Journal of Veterinary Science
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• v.22 no.3
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• pp.25.1-25.16
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• 2021

Background: Malignant lymphoma is the most common hematopoietic malignancy in dogs, and relapse is frequently seen despite aggressive initial treatment. In order for the treatment of these recurrent lymphomas in dogs to be effective, it is important to choose a personalized and sensitive anticancer agent. To provide a reliable tool for drug development and for personalized cancer therapy, it is critical to maintain key characteristics of the original tumor. Objectives: In this study, we established a model of hybrid tumor/stromal spheroids and investigated the association between canine lymphoma cell line (GL-1) and canine lymph node (LN)-derived stromal cells (SCs). Methods: A hybrid spheroid model consisting of GL-1 cells and LN-derived SC was created using ultra low attachment plate. The relationship between SCs and tumor cells (TCs) was investigated using a coculture system. Results: TCs cocultured with SCs were found to have significantly upregulated multidrug resistance genes, such as P-qp, MRP1, and BCRP, compared with TC monocultures. Additionally, it was revealed that coculture with SCs reduced doxorubicin-induced apoptosis and G2/M cell cycle arrest of GL-1 cells. Conclusions: SCs upregulated multidrug resistance genes in TCs and influenced apoptosis and the cell cycle of TCs in the presence of anticancer drugs. This study revealed that understanding the interaction between the tumor microenvironment and TCs is essential in designing experimental approaches to personalized medicine and to predict the effect of drugs.

• BMB Reports
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• v.32 no.2
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• pp.140-146
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• 1999

When murine fibrosarcoma L929 cells, a TNF-sensitive cell line, were treated with recombinant human tumor necrosis factor-$\alpha$ (rhTNF-$\alpha$), the activities of glycolytic regulatory enzymes and lactate dehydrogenase increased up to 100-150% compared to the control L929 cells after TNF treatment. By using various metabolic inhibitors and activators, it was found that cAMP-dependent protein kinase is responsible for the increase of activities of the glycolytic enzymes. The activities of glycolytic regulatory enzymes and lactate dehydrogenase of TNF-resistant A549 cells, a human lung carcinoma cell line, did not increase significantly compared to TNF-sensitive L929 cells upon TNF treatment. In contrast, the pyruvate carboxylase activities of A549 cells, but not L929 cells, increased up to 30~40% after TNF treatment. The data suggest that pyruvate carboxylase activity may contribute to the compensation of energy loss mediated by TNF treatment in TNF-resistant A549 cells.

• YAKHAK HOEJI
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• v.48 no.2
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• pp.147-152
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• 2004

A wide variety of cancer chemotherapeutic agents have been shown to induce programmed cell death (PCD, APOPTOSIS) in various tumor cell lines in vitro. cis-Malonato [(4R,5R)-4,5-bis(aminomethyl)-2-isoprpopyl-1,3-dioxolane] platinum(II) (heptaplatin), which is a new drug approved by KFDA in 1999, in a novel platinum-based antitumor agent with clinical potential against stomach cancer and the 3rd generation of the cisplatin. This study was performed to know how heptaplatin and cisplatin and sunpla (mixture of heptaplatin and mannitol) affect on SK-MEL-28 cell line, and how they induce the apoptosis. At EM analysis, the morphology of the cell was changed by treatment of the cisplatin, heptaplatin and sunpla. Apoptotic body formed around plasma membrane, and chromatin condensation represented in nucleus. This phenomenon is one of the characteristic of the apoptosis. The DNA of SK-MEL-28 cell line truncated by cisplatin and sunpla treatment was identified on 2% agarose gel electrophoresis. TUNEL assay was performed to know whether SK-MEL-28 cell die as apoptosis or necrosis by cisplatin, heptaplatin and sunpla. At this result, fluorescence intensity increased according to increase of time and concentration. Therefore, it was identified that cislatin, heptaplatin and sunpla induced apoptosis. Fas expressed on SK-MEL-28 cell membrane by cisplatin, heptaplatin and sunpla was identified by using flow cytometer and the expression of bcl-2(anti-apoptotic gene) decreased according to increase of concentration of the cisplatin, heptaplatin and sunpla. Cisplatin, heptaplatin and sunpla induced apoptosis against SK-MEL-28 cell line, and the apoptotic mechanism was identified as Fas-mediated apoptosis and decreased bcl-2 expression.

• Biomedical Science Letters
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• v.28 no.3
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• pp.200-205
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• 2022

Established cancer cell lines are widely used for developing biomarkers for the patient-specific treatment of colorectal cancer and predicting prognoses. However, cancer cell lines may exhibit different drug responses depending upon the characteristics of the cell line. Therefore, it is necessary to select a tumor cell line suitable for the purpose of the study by considering the cell characteristics. This study investigated the levels of CXCL10, which were recently been reported to play an important role in the outcome of tumor treatment, secreted by colon cancer cells. 2 × 10⁵ cells/mL of each colorectal cancer cell was seeded into a 35 mm cell culture dish. After 24 h incubation, culture supernatant was used to determine the secreted CXCL10 levels. Among six colorectal cancer cell lines (HT-29, HCT116, CaCo-2, SW620, SW480, and CT26), Caco-2 cells showed the highest level of CXCL10 secretion. HT-29 cells showed the second-highest level of CXCL10 secretion. No significantly measurable level of CXCL10 secretion was detected in HCT116 cells. These results will be helpful in investigating the molecular basis of colorectal cancer.

• Journal of Korean Neurosurgical Society
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• v.61 no.5
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• pp.633-639
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• 2018

Objective : We investigated the outcomes of repeat stereotactic radiosurgery (SRS) for metastatic brain tumors that locally recurred despite previous SRS, focusing on the tumor control. Methods : A total of 114 patients with 176 locally recurring metastatic brain tumors underwent repeat SRS after previous SRS. The mean age was 59.4 years (range, 33 to 85), and there were 68 male and 46 female patients. The primary cancer types were non-small cell lung cancer (n=67), small cell lung cancer (n=12), gastrointestinal tract cancer (n=15), breast cancer (n=10), and others (n=10). The number of patients with a single recurring metastasis was 95 (79.8%), and another 19 had multiple recurrences. At the time of the repeat SRS, the mean volume of the locally recurring tumors was 5.94 mL (range, 0.42 to 29.94). We prescribed a mean margin dose of 17.04 Gy (range, 12 to 24) to the isodose line at the tumor border primarily using a 50% isodose line. Results : After the repeat SRS, we obtained clinical and magnetic resonance imaging follow-up data for 84 patients (73.7%) with a total of 108 tumors. The tumor control rate was 53.5% (58 of the 108), and the median and mean progression-free survival (PFS) periods were 246 and 383 days, respectively. The prognostic factors that were significantly related to better tumor control were prescription radiation dose of 16 Gy (p=0.000) and tumor volume less than both 4 mL (p=0.001) and 10 mL at the repeat SRS (p=0.008). The overall survival (OS) periods for all 114 patients after repeat SRS varied from 1 to 56 months, and median and mean OS periods were 229 and 404 days after the repeat SRS, respectively. The main cause of death was systemic problems including pulmonary dysfunction (n=58, 51%), and the identified direct or suspected brain-related death rate was around 20%. Conclusion : The tumor control following repeat SRS for locally recurring metastatic brain tumors after a previous SRS is relatively lower than that for primary SRS. However, both low tumor volume and high prescription radiation dose were significantly related to the tumor control following repeat SRS for these tumors after previous SRS, which is a general understanding of primary SRS for metastatic brain tumors.