• Asian Pacific Journal of Cancer Prevention
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• v.14 no.2
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• pp.765-768
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• 2013

Background and Aims: Prostate cancer is the most commonly diagnosed cancer in males in many populations. Metformin is the most widely used anti-diabetic drug in the world, and there is increasing evidence of a potential efficacy of this agent as an anti-cancer drug. Metformin inhibits the proliferation of a range of cancer cells including prostate, colon, breast, ovarian, and glioma lines. MicroRNAs (miRNAs) are a class of small, non-coding, single-stranded RNAs that downregulate gene expression. We aimed to evaluate the effects of metformin treatment on changes in miRNA expression in PC-3 cells, and possible associations with biological behaviour. Materials and Methods: Average cell viability and cytotoxic effects of metformin were investigated at 24 hour intervals for three days using the xCELLigence system. The $IC_{50}$ dose of metformin in the PC-3 cells was found to be 5 mM. RNA samples were used for analysis using custom multi-species microarrays containing 1209 probes covering 1221 human mature microRNAs present in miRBase 16.0 database. Results: Among the human miRNAs investigated by the arrays, 10 miRNAs were up-regulated and 12 miRNAs were down-regulated in the metformin-treated group as compared to the control group. In conclusion, expression changes in miRNAs of miR-146a, miR-100, miR-425, miR-193a-3p and, miR-106b in metformin-treated cells may be important. This study may emphasize a new role of metformin on the regulation of miRNAs in prostate cancer.

• Journal of Nutrition and Health
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• v.29 no.2
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• pp.192-198
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• 1996

This experiment was conducted to examine the effects of fish oil supplementation with low does on the lipid concentration and fatty acid composition of plasma and the fatty acid composition of plasma phospholipid and erythrocyte of infants. Among 18 breast-fed infants, 6 were in control group and 12 were in fish oil groups. The subjects in fish oil groups were nursed by their mothers who supplemented with fish oil 1.96g/d or 3.92g/d, respectively for 2 weeks from 10 to 12 weeks postpartum. The nursing mothers consumed their usual diets at home. Blood samples were collected at the final day of experiment. There were no significant changes in daily intakes of total lipid, triglyceride, free fatty acid, phospholipid and cholesterol of infants by fish oil supplementation. However, the content of EPA (eicosapentaenoic acid)increased and that of ARA (arachidonic acid) decreaed significantly in plasma PC(phophatidylchline). And also, there were tendencies to increase triglyceride concentration and to decrease cholesterol and phopholipid concentrations of plasma. As the above results, atherogenic index (AI) showed a tendency to decrease, but not significant. DHA (docosahexaenoic acid) and EPA contents in plasma PC and PE (phosphatidylethanolamin) as well as those of erythrocyte tended to increase. In these results, we concluded that fish oil supplementation with low dose to lactating women does not obviously affect of the plasma lipid concentrations and fatty acid composition of plasma PC and PE as well as erythrocyte. However the increase of EPA content of plasma PC and the tendency to increase DHA and EPA contents of plasma as well as erythrocyte membrane indicate that there may be some beneficial effect on infant lipid metabolism of fish oil intake of nutsing mother were increased.

• Journal of Nutrition and Health
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• v.29 no.2
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• pp.213-222
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• 1996

The most abundant long-chain polyunsaturated fatty acid in brain lipids is docosahexaenoic acid(C22 : 6 N-3, DHA). It is incorporated into nerve tissues mostly in utero and during the first year of life. DHA in brain is derived from either pre-formed DHA in human milk or by infant hepatic synthesis from linolenic acid in milk. This study was designed to investigate the effects of DHA supplementation on fatty acid profiles in maternal plasma lipid and breast milk. Twenty lactating women participated in the study. Seven women took 3g of fish oil per day and vitamin E for 28 days starting from the day of giving birth. Five women consumed 1.5g of fish oil as well as tivamin E, and the rest took vitamin E supplements for the same period of time. Dietary questionnaires and 3 consecutive 24-h recalls were collected to evaluate theri nutritional status and food habits. Finding that DHA intake from fish was not significantly different among three experimental groups, the partcipants were instructed to continue eating their usual home diets. Milk samples were taken on the day of giving birth, as well as the 7th, 14th and 28th day being the supplement phase, and finally 2 weeks after the cessating of DHA supplements. The amounts of the fish oil supplements produced significant dose-dependent increased in the DHA content of milk and plasma, but to a lesser degree. Base-line for 28 days raised the level to 2.05$\pm$0.43% and 1.5g/day supplement produced DHA levels of 1.02$\pm$0.19%. The results of this study indicated that relatively small amount of dietary DHA supplementation significantly elevats DHA content in milk. This would clearly elevate the infant's DHA intake which in turn may have implications for the infant's brain development.

• KSBB Journal
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• v.18 no.5
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• pp.424-428
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• 2003

In the present study, we have analyzed effects of the endocrine distruptors, such as bisphenol A, nonylphenol and pentachlorophenol, on cell proliferation in the human breast cancer cell line, MCF-7, and the human prostate cancer cell line, PC-3, with MTT method. A dose dependent analysis of the cell proliferation of MCF-7 cells after administration of bisphenol A, nonylphenol and pentachlorophenol revealed a significant induction of cell proliferation. Maximum induction of cell proliferation was observed at concentrations between 10$\^$-7/ and 10$\^$-6/ M. Whereas, these chemicals had little effect on proliferation of PC-3 cells. These results demonstrated that bisphenol A, nonylphenol and pentachlorophenol do not induce proliferation of PC-3 cells but exhibit a significant induction of MCF-7 cell proliferation, suggesting all these chemicals are a estrogen mimic.

• Food Science of Animal Resources
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• v.32 no.5
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• pp.612-617
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• 2012

The antioxidant, antimicrobial, and cytotoxic activities of ovotransferrin were investigated in vitro. The antioxidant capacity of ovotransferrin was evaluated using the 2,2-Diphenyl-1-picryl hydrazyl (DPPH) radical scavenging method, antimicrobial effects using the agar well diffusion method, and cytotoxicity using the 3-(4,5-dimethylthizol-2-yl)-2,5-diphenylatetetrazolium bromide (MTT) assay. The DPPH radical-scavenging capacity of ovotransferrin at 1 mg/mL level reached approximately 60% after 48 h of reaction. The antimicrobial effects of ovotransferrin against common food-borne pathogens, Staphylococcus aureus KCCM 32395, Bacillus cereus KCCM 40935, Listeria monocytogenes ATCC 15313, Escherichia coli O157:H7 ATCC 43895, and Helicobacter pylori HpKCTC 26695 were dose dependant. Gram-positive bacteria was more sensitive to ovotransferrin than gram-negative bacteria. Ovotransferrin showed stronger antimicrobial effect against L. monocytogenes than other gram-positive bacteria tested. The cytotoxicity of ovotransferrin was evaluated in human cancer cell lines, various tissue origins, including the larynx (Hep-2), stomach (AGS), lung (SK-MES-1), liver (HepG2), breast (MCF-7), cervix (HeLa), and colon (HT-29). Ovotransferrin displayed relatively high cytotoxicity (${\leq}60%$ inhibition effects) at 40 mg/mL. At lower concentrations (${\leq}10mg/mL$), however, ovotransferrin cytotoxic effects were not significant in all cancer cell lines tested. These results indicated that ovotransferrin has potential to be used as an antioxidant or antimicrobial agent in foods or a pharmaceutical agent against cancers.

• Radiation Oncology Journal
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• v.5 no.2
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• pp.119-129
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• 1987

With the introduction of X-rays of higher energy that have higher penetrability, it has become possible to treat the deep-seated tumor with increased local control rate. But at the same time it has incrased the damage to the deep seated organs, especially to the lung which is known to be the less radiotolerable tissue in the body. This study analyses the 66 patients who were exposed to the irradiation of the lung, and examines the development of radiation pneumonitis and its related factors. The results of the study are summarized as follows: 1, The 66 patients were consisted of 40 cases of lung cancer, 15 cases of breast cancer and 11 cases of mediastinal tumors. There were 37 males and 29 females with the male to female ratio 1.3: 1. A male to female ratio in the lung cancer was 3: 1. 2. Among 66 patients, 26 patients $(39\%)$ developed the radiographical changes of acute radiation pneumonitis and 13 out of 26 patients $(50\%)$ showed the clinical features of acute radiation pneumonitis. 3. The onest of acute radiation pneumonitis ranged from 10 days to 6 months after the completion of radiotherapy. 4. There was a statistically significant close relationship between the development of radiation pneumonitis and the radiation dose. 5. As the irradiated lung volume increased, the development of radiation pneumonitis increased. But the statistical significance was not strong. 6. The increased incidence of radiation pneumonitis was observed when the chemotherapy was given before or concomittantly with radiotherapy. 7 There was no significant correlation between the development of radiation pneumonitis and the age, smoking and the presence of underlying lung disease.

• Environmental Mutagens and Carcinogens
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• v.24 no.4
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• pp.163-170
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• 2004

CYP1B1 enzyme metabolize PAHs and estradiol. CYP1B1 metabolize estradiol to 4-hydroxyestradiol that is considered as carcinogenic metabolite. Luciferase activity was induced about 20 folds over that control by 1 nM TCDD (2,3,7,8-tetrchlorodibenzo-p-dioxin) and these inductions were dose-dependent. Recent industrialized society, human hasbeen widely been exposed to widespread environmental contaminants such as PAHs (polycyclic aromatic hydrocarbon) that are originated from the incomplete combustion of hydrocarbons. PAHs are known to be ligands of the AhR (aryl hydrocarbon receptor). Induction of cytochrome P4501B1(CYP1B1) in cell culture is widely used as a biomarket for PAHs. Therefore we have studied the effect of PAHs in the human breast cancer cells MCF-7 to evaluate bioactivity of PAHs. Cytochrome P4501B1(CYP1B1) is known to be inducible by xenobiotic compounda such as policyclic aromatic hydrocarbon (PAH) and dioxins such as 2,3,7,8-tetrachloro-dibenzo-p-dioxin(TCDD). And these induction of CYP1B1 is also regulated by many categories of chemicals. In order to investigate the effects of several chemicals on CYP1B1 gene expression in luciferase gene, and then transfected into these cells. After treatment of chemicals, the luciferase activity was measured. We examined effects of PAHs on the CYP1B1-lucifrease reporter gene and CYP1B1 mRNA level. Benzo(k)fluoranthene showed strong response to CYP1B1 promoter activity stimulation, and also CYP1B1 mRNAs increase in MCF-7 cells in a concentration-dependent manner. flvonoids such as genistein decreased B(k)F induced luciferase activity at low concentration. it exhibited stimulatory effect at high concentration.

• Journal of Radiation Protection and Research
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• v.42 no.4
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• pp.177-188
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• 2017

Background: Radiation-induced pneumonitis and pulmonary fibrosis are common dose-limiting complications in patients receiving radiotherapy for lung, breast, and lymphoid cancers. In this study, we investigated the characteristics of effective immune cells related to pneumonitis and fibrosis after irradiation. Materials and Methods: After anesthesia, the whole thorax of C57BL/6 mice was irradiated at 14 Gy. The lung tissue and bronchoalveolar lavage fluid were collected at defined time points post-irradiation for the determination of histological and immunohistochemical analysis and inflammatory cell population infiltrated into the lung. Results and Discussion: Whole thoracic irradiation increased the deposition of extracellular matrix (ECM), lung weight, and pleural effusions, which started to die from 4 months later. At 4 months after irradiation, the numbers of macrophages and lymphocytes as well as neutrophils were increased dramatically in the lung. Interestingly, the macrophages that were recruited into the lung after irradiation had an enlarged foamy morphology. In addition, the expressions of chemokines (CCL-2, CCL-3, CXCL-10) for the attraction of macrophages and T cells were higher in the lung of irradiated mice. The high expressions of these chemokines were sustained up to 6 months following irradiation. In thoracic irradiated mice, infiltrated macrophages into the lung had the high levels of Mac-3 antigens on their surface and upregulated the hallmarks of alternatively activated macrophages such as arginase-1 and CD206. Furthermore, the levels of IL-4 and IL-13 were higher in a BAL fluid of irradiated mice. Conclusion: All results show that thoracic irradiation induces to infiltrate various inflammation-related immune cells, especially alternatively activated macrophages, through enhancing the expression of chemokines, suggesting that alternatively activated macrophages are most likely important for leading to pulmonary fibrosis.

• Korean Journal of Environmental Biology
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• v.23 no.1
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• pp.21-26
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• 2005

Cell response to genotoxic agents is complex and involves the participation of different classes of genes including cell cycle control, DNA repair and apoptosis. In this report, we presented a approach to characterize the cellular functions associated with the altered transcript profiles of MCF-7 exposed to low-dose in vitro gamma-irradiation. We used the method of human 2.4 k cDNA microarrays containing apoptosis, cell cycle, chromatin, repair, stress and chromosome genes to analyze the differential gene expression characterization that were displayed by radiation-exposed cell, human breast carcinoma MCF-7 cell line, such as 4 Gy 4 hr, 8 Gy 4 hr, and 8 Gy 12 hr. Among these genes, 66 were up-regulated and 49 were down-regulated. Specific genes were concomitantly induced in the results. Cyclin dependent kinase 4 (Cdk4) is induced for starting the cell cycle. This regulation is required for a DNA damage­induced G1 arrest. In addition to, an apoptotic pathways gene Bcl-w was concomitantly induced. Mismatch repair protein homologue-l (hMLH1), a necessary component of DNA mismatch protein repair (MMR), in G2-M cell cycle checkpoint arrest. The present study provides new information on the molecular mechanism underlying the cell response to genotoxic stress, with relevance to basic and clinical research.

• Journal of Radiopharmaceuticals and Molecular Probes
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• v.1 no.2
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• pp.130-136
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• 2015

We evaluate the influence of MR contrast agent on positron emission tomography (PET) image using phantom, animal and human studies. Phantom consisted of 15 solutions with the mixture of various concentrations of Gd-based MR contrast agent and fixed activity of [$^{18}F$]FDG. Animal study was performed using rabbit and two kinds of MR contrast agents. After injecting contrast agent, CT or MRI scanning was performed at 1, 2, 5, 10, and 20 minutes. PET image was obtained using clinical PET/CT scan, and attenuation correction was performed using the all CT images. The values of HU, PET activity and MRI intensity were obtained from ROIs in each phantom and organ regions. In clinical study, patients (n=20) with breast cancer underwent sequential acquisitions of early [$^{18}F$]FDG PET/CT, MRI and delayed PET/CT. In phantom study, as the concentration increased, the CT attenuation and PET activity also increased. However, there was no relationship between the PET activity and the concentration in the clinical dose range of contrast agent. In animal study, change of PET activity was not significant at all time point of CT scan both MR contrast agents. There was no significant change of HU between early and delayed CT, except for kidney. Early and delayed SUV in tumor and liver showed significant increase and decrease, respectively (P<0.05). Under the condition of most clinical study (< 0.2 mM), MR contrast agent did not influence on PET image quantitation.