전립선암의 정확한 진단을 위한 질감 특성 분석 및 등급 분류

김초희(Cho-Hee Kim),소재홍(Jae-Hong So),박현균(Hyeon-Gyun Park),Nuwan Madusanka,Prakash Deekshitha,Subrata Bhattacharjee,최흥국(Heung-Kook Choi) 한국멀티미디어학회 2019 멀티미디어학회논문지 Vol.22 No.8

Combined Treatment of Nonsteroidal Anti-inflammatory Drugs and Genistein Synergistically Induces Apoptosis via Induction of NAG-1 in Human Lung Adenocarcinoma A549 Cells

Cho Hee Kim(김초희),Min Young Kim(김민영),Su Yeon Lee(이수연),Ji Young Moon(문지영),Song Iy Han(한송이),Hye Gyeong Park(박혜경),Ho Sung Kang(강호성) 한국생명과학회 2009 생명과학회지 Vol.19 No.8

비스테로이드성 항염증약(nonsteroidal anti-inflammatory drugs; NSAIDs)은 항염 및 진통효과를 나타내며, 염증억제 외에 다양한 신호전달 분자를 통해 여러 가지 세포생리활성을 조절하며, 암세포에서는 세포사멸 유도를 통한 항암제 효과를 보이고 있다. 본 연구에서는 NSAIDs가 암세포사멸프로그램을 작동시키는데 있어 phosphatidyl inositol 3-kinase (PI3K)-Akt/protein kinase B (PKB) 그리고 MEK1/2-ERK1/2 신호 전달계과 같은 antiapoptotic program이 NSAIDs의 효과를 경감시키는 것으로 예상하고, 이들 항세포사멸 프로그램을 억제하였을 경우, NSAIDs의 세포사멸 유도작용이 증가되는지 그 가능성을 조사하였다. 세포사멸은 Hoeschst 33342으로 핵응축과 핵 쪼개짐을 염색하여 확인하였다. Western blotting을 통해 단백질 발현과 역전사중합효소연쇄반응을 통해 mRNA 발현을 확인하였다. NSAIDs 처리와 동시에 PI3K-Akt/PKB와 MEK-ERK1/2 신호전달계의 억제제를 함께 처리했을 때, NSAIDs의 세포사멸유도작용이 증가함을 확인하였다. 또한 PI3K와 MEK1/2 신호전달계의 상위에 존재하는 receptor tyrosine kinases (RTKs)의 억제제인 genistein을 함께 처리하였을 때에도 유사한 효과가 나타남을 확인하였다. 그리고 이들 복합처리에 의해 NAG-1 발현이 증가하며 NAG-1 interference 하였을 경우 복합처리에 의한 세포사멸증진 효과가 사라짐을 확인하였다. 본 연구결과는 암세포에 활성화 되어 있는 세포생존 프로그램을 제어하는 물질(genistein 혹은 LY294002+U0126)을 복합처방함으로써 NSAIDs의 항암작용을 증진시킬 수 있음을 보여준다. A number of studies have demonstrated that the regular use of nonsteroidal anti-inflammatory drugs (NSAIDs) can reduce the risks of colorectal, oesophageal and lung cancers. NSAIDs have been shown to exert their anti-cancer effects through inducing apoptosis in cancer cells. The susceptibility of tumor cells to anti-tumor drug-induced apoptosis appears to depend on the balance between pro-apoptotic and anti-apoptotic programs such as nuclear factor kB (NF-kB), phosphatidylinositol 3-kinase (PI3K)-Akt/protein kinase B (PKB) and MEK1/2-ERK1/2 pathways. We examined the effects of pro-survival PI3K and ERK1/2 signal pathways on cell cycle arrest and apoptosis in response to NSAIDs including sulindac sulfide and NS398. We show that simultaneous inhibition of the Akt/PKB and ERK1/2 signal cascades could synergistically enhance the potential pro-apoptotic activities of sulindac sulfide and NS398. Similar enhancement was observed in cells treated with sulindac sulfide or NS398 and 100 μM genistein, an inhibitor of receptor tyrosine kinases (RTKs) that are upstream of PI3K and MEK1/2 signaling. We further demonstrate that NAG-1 is induced and plays a critical role(s) in apoptosis by NSAIDs-based combined treatment. In sum, our results show that combinatorial treatment of sulindac sulfide or NS398 and genistein results in a highly synergistic induction of apoptotic cell death to increase the chemopreventive effects of the NSAIDs, sulindac sulfide and NS398.

호기성 그래뉼을 이용한 유기물 및 질소제거 효율에 관한 연구

김초희 ( Cho Hui Kim ),( Yu Hong Jia ),류재훈 ( Jae Hun Ryu ),이우경 ( Woo Kyung Lee ),( Tran Thi Van Trinh ),안대희 ( Dae Hee Ahn ) 한국물환경학회 ( 구 한국수질보전학회 ) 2010 공동 추계학술발표회 Vol.2010 No.-

텍스트마이닝을 활용한 시대별 K-POP 동향 분석: 언론보도를 중심으로

김욱동(Kim Ouk-Dong),김현진(Kim Hyun-Jin),김초희(Kim Cho-Hee) 한국실용무용학회 2023 한국실용무용학회지 Vol.1 No.2

In this paper, big data analysis has been conducted using text mining, focusing on domestic K-pop-related news press releases for the past 33 years. Research questions were set on the trends of K-pop by era divided into four categories and the implications of the analysis results. For data analysis, 129,062 K-pop-related press releases from January 1, 1990 to December 31, 2022 were collected using the BigKinds data analysis platform, and data preprocessing and analysis were conducted through text mining modules that can be used in the Python environment. The analysis results are as follows. The main keywords of the first K-pop period were "love," "America," "Japan," "culture," and "rock." The main keywords of the second K-pop group were "Japan," "Love," "America," "Promotion," and "Movie." The main keywords of the third K-pop generation were "idol," "BTS," "entertainment," "Today," and "love." The main keywords of the 4th K-pop group were 'idol', 'trot', 'BTS', 'corona', and 'entertainment'. After that, the final discussion points were derived by comparing the researcher's interpretation with various references through discussions between researchers focusing on the analysis results. This study is meaningful in that it provides quantitative academic data in the field of K-pop. 본 논문에서는 지난 33년간 국내 케이팝(K-POP) 관련 뉴스 보도자료를 중심으로 텍스트마이닝 분석방법을 활용, 빅데이터 분석을 진행하였다. 4개로 구분된 시대별 케이팝의 동향, 그리고 그 분석결과가 가지는 시사점에 대해 연구문제를 설정하였다. 자료 분석을 위해 빅카인즈(BigKinds) 데이터분석 플랫폼을 이용하여 1990년 1월 1일부터 2022년 12월 31일까지의 케이팝 관련 보도자료 129,062건을 수집하였고, 파이썬 환경에서 활용할 수 있는 텍스트마이닝 모듈을 통해 데이터 전처리 및 분석을 진행하였다. 그 분석결과는 다음과 같다. 케이팝 1기의 주요 키워드로는 ‘사랑’, ‘미국’, ‘일본’, ‘문화’, ‘록’ 등으로 나타났다. 케이팝 2기의 주요 키워드로는 ‘일본’, ‘사랑’, ‘미국’, ‘홍보’, ‘영화’ 등으로 나타났다. 케이팝 3기의 주요 키워드로는 ‘아이돌’, ‘방탄소년단’, ‘예능’, ‘투데이’, ‘사랑’ 등으로 나타났다. 케이팝 4기의 주요 키워드로는 ‘아이돌’, ‘트로트’, ‘방탄소년단’, ‘코로나’, ‘예능’ 등으로 나타났다. 이후 분석 결과를 중심으로 연구자 간 논의를 거쳐 연구자의 해석을 다양한 참고문헌들과 대조하며 최종 논의점을 도출하였다. 본 연구는 케이팝 분야의 정량적 학술자료를 제공하였다는 데 있어 의의를 가진다.

수류 환경 볼 베어링 모재 SUS440C 위에 코팅된 고체 윤활제의 마찰 마모 특성 평가

서우석(Wooseok Seo),김초희(Cho-Hee Kim),최복성(Bok Seong Choi),류솔지(Sol Ji Ryu),이병국(Byung Kok Lee),이용복(Youngbok Lee),이전국(Jeon-Kook Lee) 대한기계학회 2014 대한기계학회 춘추학술대회 Vol.2014 No.4-1

Combined Treatment of Sodium Salicylate and Genistein Induces Incomplete Apoptosis and Necrosis in MCF-7 Multicellular Tumor Spheroids

Su Yeon Lee(이수연),Cho Hee Kim(김초희),Hyun Min Jeon(전현민),Min Kyung Ju(주민경),Min Young Kim(김민영),Eui-kyong Jeong(정의경),Hye Gyeong Park(박혜경),Ho Sung Kang(강호성) 한국생명과학회 2012 생명과학회지 Vol.22 No.9

아스피린과 아스피린의 deacetylated form인 sodium salicylate (NaSal)은 대장암, 폐암 및 유방암을 비롯한 다양한 암의 항암제 활성을 나타내는 것으로 잘 알려져 있다. A549 폐암 세포주에 저농도의 NaSal과 genistein을 함께 복합 처리시 상승작용에 의해 세포사멸을 증가시켜서 NaSal에 의한 암억제 효과를 증대시킴을 이미 밝힌 바 있다. 본 연구에서는 A549가 아닌 다른 암세포주와 in vitro solid tumor model인 multicellular spheroids (MTS)을 이용하여 NaSal과 genistein 복합처리 효과를 조사하였다. NaSal/genistein 복합 처리시 A549 세포주와 마찬가지로 HCT116 세포주에서도 세포사멸이 유도되었지만, MCF-7 세포주에서는 유도되지 않았다. 흥미롭게도, MCF-7 세포주는 MTS로 배양되는 동안 NaSal/genistein 복합 처리에 의해 세포 죽음을 나타내었다. 세포 죽음의 형태는 MCF-7 MTS의 발달 단계에 따라 세포사멸 또는 세포괴사로 나타났다. MCF-7 MTS에서의 세포사멸은 불완전한 양상을 보였다. 즉 염색체가 응축되고 쪼개지지만, 핵막은 여전히 관찰되었다. 이상의 연구 결과 NaSal/genistein 복합처리는 MCF-7 MTS 배양 system에서 불완전한 세포사멸과 세포괴사를 일으킴을 알 수 있었다. Aspirin and its deacetylated form, sodium salicylate (NaSal), have been shown to exert chemopreventive activities against many human cancers including those of the colon, lung, and breast. Previously, we showed that combined treatment of NaSal and genistein synergistically induced apoptosis in A549 lung cancer cells, indicating that these two natural chemicals could be used in combination for cancer therapy. In this study, we examined effects of NaSal/genistein combined treatment on other cancer cells and in three-dimensional multicellular tumor spheroid (MTS) and in an in vitro solid tumor model. We found that the combined treatment induces apoptosis in the HCT116 cells and the A549 cells, but not in the MCF-7 cells. Interestingly, the MCF-7 cells responded to the NaSal/genistein combined treatment by undergoing cell death when they were cultivated as MTS. The combined treatment induced apoptosis at an earlier stage in the MCF-7 MTS culture. However, when the MCF-7 MTS was cultivated for a longer period, it induced necrosis rather than apoptosis. We further found that the apoptotic pattern observed in MCF-7 MTS was incomplete: the chromatins were condensed and fragmented, but the nuclear membrane was still intact. Taken together, these results demonstrate that the NaSal/genistein combined treatment induces incomplete apoptosis and necrosis in the MCF-7 MTS culture system.

중형규모 아파트 거주자의 공간이용방식과 주요구

박경옥(Kyoung Ok Park),김초희(Cho Hee Kim),김지혜(Ji Hye Kim),이은주(Eun Ju Lee) 충북대학교 생활과학연구소 2009 생활과학연구논총 Vol.13 No.2

This study has its purpose to make planning criteria to the most highly preferred apartment plans with size of 85 to 100㎡. The 96 housewives residing in Cheongju city answered the questionnaire on their living activities and needs on the spaces of apartment. The frequency analysis of the questionnaire showed the following result. The ‘anbang' was the space only for the individual living activities of husband and wife, whereas the living room was the space for various activities like sleeping, rest and hobby. The kitchen-dining room was the space for dining and chattering, and the dining space was used for guest reception. The living room was where non-routine activities occur. The standing-sitting activity rate was most highly found at children’s room, and found sequentially lower at dinning room, living room, and ‘anbang'. The most preferred plan was that of independent living room, and of the kitchen with dinning space.

감염의 확산 방지를 위한 종합병원 설계

한은비(Han, Eun-Bee),최필선(Choi, Pil-Seon),김초희(Kim, Cho-Hee),이현진(Lee, Hyun-Jin) 한국생태환경건축학회 2017 한국생태환경건축학회 학술발표대회 논문집 Vol.17 No.2

Snail Switches 5-FU-induced Apoptosis to Necrosis through Akt/PKB Activation and p53 Down-regulation

Su Yeon Lee(이수연),Hyun Min Jeon(전현민),Min Kyung Ju(주민경),Cho Hee Kim(김초희),Eui-kyong Jeong(정의경),Hye Gyeong Park(박혜경),Ho Sung Kang(강호성) 한국생명과학회 2012 생명과학회지 Vol.22 No.8

Snail은 E-cadherin 발현을 직접 억제하는 zinc finger transcription factor로서, 암세포의 invasion과 metastasis를 촉진시키는 epithelial-mesenchymal transition (EMT)를 유발한다. 또한 Snail은 세포사멸 자극과 세포 생존물질의 제거로 인한 세포사멸에 대해 저항성을 나타낸다. 그러나 이에 대한 분자기작은 잘 알려져 있지 않다. 본 연구에서는 가장 널리 사용되는 항암제 중의 하나인 5-fluorouracil (5-FU)에 의한 세포사멸에 대한 Snail의 저항성 기작에 대하여 조사하였다. MCF-7 #5 세포주에 doxycycline (DOX)을 처리하여 Snail을 과발현시킨 세포에서 5-FU에 의한 세포사멸이 억제되고 세포괴사가 일어남을 확인하였다. DOX 처리 및 Snail expression vectors인 pCR3.1-Snail-Flg와 phosphorylation-resistant mutant Snail vector인 pCR3.1-S104, 107A Snail-Flg을 이용하여 Snail을 과발현 시킨 경우 ERK1/2의 활성에는 영향을 주지 않는 반면 PTEN 발현억제 및 불활성화, 그리고 Akt/PKB 활성화가 유도됨을 관찰하였다. 또한, Snail은 5-FU에 의한 p53의 발현을 억제한다는 사실을 확인하였다. 따라서 Snail은 prosurvival kinase인 Akt/PKB의 활성화와 p53 억제를 통해 5-FU에 의한 세포사멸을 세포괴사로 전환하는 것으로 생각된다. Snail is a zinc finger transcription factor that induces epithelial-to-mesenchymal transition (EMT), which promotes tumor invasion and metastasis by repressing E-cadherin expression. In addition, Snail restricts the cellular apoptotic response to apoptotic stimuli or survival factor withdrawal; however, its molecular mechanism remains largely unknown. In this study, we have investigated the mechanism underlying Snail-mediated chemoresistance to 5-fluorouracil (5-FU), one of the most widely used anti-cancer drugs. When Snail was overexpressed by doxycycline (DOX) in MCF-7 #5 cells, it inhibited 5-FU-induced apoptotic cell death and switched the cell death mode to necrosis. Snail expression, either by DOX treatment in MCF-7 #5 cells or by the transfection of Snail expression vectors pCR3.1-Snail-Flg, phosphorylation-resistant pCR3.1-S104, and 107A Snail-Flg in MCF-7 cells specifically induced PTEN down-regulation/inactivation and Akt/PKB activation, without affecting ERK1/2 activity. In addition, Snail prominently suppressed 5-FU-induced increases in p53 levels. These findings demonstrate that Snail switches 5-FU-induced apoptosis to necrosis through the activation of Akt/PKB and the down-regulation of p53 levels.

High-mobility Group Box 1 Induces the Epithelial-mesenchymal Transition, Glycolytic Switch, and Mitochondrial Repression via Snail Activation

Su Yeon Lee(이수연),Min Kyung Ju(주민경),Hyun Min Jeon(전현민),Cho Hee Kim(김초희),Hye Gyeong Park(박혜경),Ho Sung Kang(강호성) 한국생명과학회 2019 생명과학회지 Vol.29 No.11

암세포는 epithelial mesenchymal transition (EMT)를 통해 tumor invasion과 metastasis가 일어나며, 또한 정상세포와 다른 oncogenic metabolic phenotypes 획득 즉, glycolytic switch 등이 암 발생과 진행에 깊이 연관되어 있음이 잘 알려져 있다. High-mobility group box 1 (HMGB1)은 chromatin-associated nuclear protein으로 알려져 있으나, dying cells 또는 immune cells로부터 방출되기도 한다. 방출된 HMGB1은 damage-associated molecular pattern (DAMP)로서 작용하여 EMT 및 invasion, metastasis를 유도함으로서 tumor progression에 기여한다고 알려졌다. 본 연구에서 HMGB1에 의해 EMT와 glycolytic switch 유도되며, 이 과정은 Snail 의존적임을 확인하였다. 또한 HMGB1/Snail cascade는 COX subunits인 COXVIIa와 COXVIIc의 발현 억제를 통해 mitochondrial repression과 cytochrome c oxidase (COX) inhibition을 유도하였다. HMGB1은 Snail를 통해 glycolytic switch의 주요 효소인 hexokinase 2 (HK2), phosphofructokinase-2/fructose-2,6-bisphosphatase 2 (PFKFB2), phosphoglycerate mutase 1 (PGAM1)의 발현을 증가시켰다. 이들 효소는 glycolytic switch에 중요하게 관여하는 것으로 알려져 있다. 이들 해당과정의 효소들을 knockdown한 결과 HMGB1에 의한 EMT를 억제함으로써 glycolysis와 HMGB1-induced EMT가 밀접하게 연관되어 있을 제시하였다. 이상의 연구 결과들은 HMGB1/Snail cascade가 EMT 및 glycolytic switch, mitochondrial repression에 중요하게 작용할 것임을 시사한다. Cancer cells undergo the epithelial-mesenchymal transition (EMT) and show unique oncogenic metabolic phenotypes such as the glycolytic switch (Warburg effect) which are important for tumor development and progression. The EMT is a critical process for tumor invasion and metastasis. High-mobility group box 1 (HMGB1) is a chromatin-associated nuclear protein, but it acts as a damage-associated molecular pattern molecule when released from dying cells and immune cells. HMGB1 induces the EMT, as well as invasion and metastasis, thereby contributing to tumor progression. Here, we show that HMGB1 induced the EMT by activating Snail. In addition, the HMGB1/Snail cascade was found induce a glycolytic switch. HMGB1 also suppressed mitochondrial respiration and cytochrome c oxidase (COX) activity by a Snail-dependent reduction in the expression of the COX subunits COXVIIa and COXVIIc. HMGB1 also upregulated the expression of several key glycolytic enzymes, including hexokinase 2 (HK2), phosphofructokinase-2/fructose-2,6-bisphosphatase 2 (PFKFB2), and phosphoglycerate mutase 1 (PGAM1), in a Snail-dependent manner. However, HMGB1 was found to regulate some other glycolytic enzymes including lactate dehydrogenases A and B (LDHA and LDHB), glucose transporter 1 (GLUT1), and monocarboxylate transporters 1 and 4 (MCT1 and 4) in a Snail-independent manner. Transfection with short hairpin RNAs against HK2, PFKFB2, and PGAM1 prevented the HMGB1-induced EMT, indicating that glycolysis is associated with HMGB1-induced EMT. These findings demonstrate that HMGB1 signaling induces the EMT, glycolytic switch, and mitochondrial repression via Snail activation.