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장환형 (Large-circular) 안티센스를 이용한 난소암세포 성장 관련 유전자의 발굴
도경오 ( Kyung Oh Doh ),천근수 ( Geun Soo Chun ),심재철 ( Jae Chul Sim ),양회생 ( Hoe Saeng Yang ) 대한산부인과학회 2009 Obstetrics & Gynecology Science Vol.52 No.7
목적: 난소암의 성장에 관련된 새로운 치료목표 유전자의 발굴을 시도하였다. 연구 방법: 재조합 M13 파아지에서 유래한 단일가닥 장환형 (large-circular, LC) 안티센스 DNA를 이용하여 난소암의 성장에 관련된 유전자를 발굴하기 위해 240개의 유전자가 클로닝 된 플라스미드를 대장균에서 배양한 후 단일가닥 장환형 안티센스 DNA를 생산하였다. 생산된 장환형 안티센스를 난소암 세포주에 주입하여 각각의 유전자의 발현과 이것이 암세포의 성장을 저해하는지를 현미경과 MTT 정량으로 관찰하였다. 결과: 240개 유전자의 발현을 억제한 결과 17개의 유전자가 암세포의 성장과 관련이 있는 것으로 밝혀졌다. 이 중에는 CD44, EpCAM 등 암세포의 성장과 관련된 것으로 알려진 유전자도 있었고 이 연구를 통해 새롭게 발굴된 것들도 있었다. 결론: 다량의 안티센스를 이용하여 유효한 난소암 치료 표적을 발굴하였고 이들에 대한 더욱 자세한 연구로 새로운 항암목표물을 개발할 수 있을 것으로 기대된다. Objective: The aim of this study is to find out the genes which are related to ovarian cancer cell growth using large circular antisense library. Methods: Clones for antisense library were uni-directionally sub-cloned into pBS SK (-) vector. LC-antisense molecules were then purified from the culture supernatants of the bacterial competent cells superinfected with M13K07 helper bacteriophages. The LC-antisense library to 240 unigene clone was constructed and utilized in the identification of genes functionally involved in the growth of ovarian cancer cells. Results: The 17 numbers out of the 240 numbers of the antisense library exerted a marked inhibitory effect on the growth of SK-OV 3. Conclusion: The putative functional categorization of each gene was then conducted via public databases. These candidates may be used as target genes for drug development or adjuvant of conventional chemotherapeutic drugs.
씨름선수에서 체중 감량과 회복기의 Leptin과 PAI-1 변화
김용운,도경오,권태동,박덕일,장응찬,박소영,김종연,이석강 대한스포츠의학회 2000 대한스포츠의학회지 Vol.18 No.2
Obesity which is defined as accumulation of excess body fat, is central factor of insulin resistance syndrome. Recently, it is revealed tat adipose tissue is not simply an energy storage organ but it also secretes a variety of molecules which affect the metabolism of the whole body, those are leptin and plasminogen activator inhibitor-1(PAI-1). Therefore, leptin and PAI-1 are increased in the obese state. Leptin regulates energy homeostasis and satiety and PAI-1 regulates fibrinolytic system. For these reasons, elevated levels of leptin and PAI-1 are considered as link factors between obesity and insulin resistance syndrome. However, the exact regulating mechanism for serum levels of leptin and PAI-1 is not fully understood yet. In this study, to evaluate the regulating mechanisms of serum levels of leptin and PAI-1 according to the weight changes, we measured leptin, PAI-1, physical, metabolic, and endocrine parameters during 10 days of weight reduction and 10 days of regain period in 7 young athletes. The mean body weight change was -4.7 kg(5.0%) in the weight reduction period and -2.4 kg(2.5%) in the weight regain period compared to baseline value. Baseline level of leptin in athletes was 1.7±0.66 ng/ml, which was significantly correlated with body weight, BMI, percent body fat, body fat mass, triglyceride, insulin, and PAI-1. Baseline level of PAI-1 in athletes was 16.6±5.26 ng/ml, which was significantly correlated with body weight, BMI, triglyceride, insulin, and leptin. Leptin was decreased to 0.7±0.39(44% of the basaline value) in the weight reduction period, and increased to 1.9±0.64(119% of the baseline value) in the regain period. PAI-1 was decreased to 7.4±2.72(44% of the basaline value) in the weight reduction period, and increased to 22.8±7.33(138% of the baseline value) in the regain period. The changes of leptin during weight reduction period were significantly correlated with the changes of insulin(r=0.890, P<0.01) and triglycerides(r=0.874, P<0.01). The changes of PAI-1 during weight reduction period were significantly correlated with the changes of FFA(r=0.889, P<0.01) and triglycerides(r=0.869, P<0.05). The changes of both leptin and AAI-1 during weight regain period were significantly correlated with the changes of insulin(r=0.755 and 0.849, P<0.05, respectively). In summary, these results suggest that serum levels of leptin and PAI-1 were affected by weight cycling, the percentages of change were more greater than that of weight change, and rebound phenomena were occurred during weight regain period.