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Drosophila Med6 is required for proliferation and metabolism associated with larval metamorphosis
Gim, Byung Soo,Park, Jin Mo,Yoon, Jeong Ho,Kang, Chang Won,Kim, Young-Joon 이화여자대학교 세포신호전달연구센터 2001 고사리 세포신호전달 심포지움 Vol. No.3
Mediator of transcriptional regulation is the evolutionary conserved co activator complex that plays the central role in the integration and recruitment of diverse regulatory signals and transcription machinery to certain promoters. In yeast, each Mediator subunit is required for transcriptional regulation of a distinct group of genes. In order to elucidate the functions of metazoan Mediator proteins, we isolated mutants of a conserved Mediator subunit, Drosophila Med6(dMed6). dMed6 null homozygotes failed to pupate and died in the third larval instar. Larval mitotic cells and most imaginal discs showed severe defects in proliferation, but no apparent morphological defect was observed in other larval tissues. Clonal analysis of dMed6 mutant cells revealed that dMed6 is essential for cell viability and proliferation of most adult cell types. Drosophila cDNA microarray, quantitative RT-PCR, and in situ expression analyses of developmentally regulated genes in dMed6 mutants showed that transcriptional activation of a subset of genes involved in cell proliferation and metabolism were most affected. Our results suggest that dMed6 is required in most cells for transcriptional regulation of a subset of genes important for cell proliferation and metabolism.
백화사설초 추출물의 인체 대장암 세포주에서 항암효능에 관한 연구
이수진,김희진,심지환,박현수,김병주,Lee, Soojin,Gim, Huijin,Shim, Ji Hwan,Park, Hyun Soo,Kim, Byung Joo 대한한의학방제학회 2015 大韓韓醫學方劑學會誌 Vol.23 No.1
Objectives : The purpose of this study was to investigate the anti-cancer effects of Oldenlandia diffusa extract on WiDr human colorectal adenocarcinoma cells. Methods : We examined cell death by (3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide) MTT assay and the caspase 3 and 9 activity assay with Oldenlandia diffusa extract. To examine the inhibitory effects of Oldenlandia diffusa extract, we performed a cell cycle (sub-G1) analysis and mitochondrial membrane potential for the WiDr cells after 24 hours with Oldenlandia diffusa extract. Results : 1. Oldenlandia diffusa extract induced cell death in WiDr cells. 2. The sub-G1 peak was increased by Oldenlandia diffusa extract in WiDr cells. 3. Oldenlandia diffusa extract leads to increase the mitochondrial membrane depolarization in WiDr cells. 4. Oldenlandia diffusa extract increases caspase 3 and 9 activities in WiDr cells. 5. Oldenlandia diffusa extract combined with several anti-cancer drugs (paclitaxel, 5-fluorouracil, cisplatin, ectoposide, doxorubicin and docetaxel) markedly inhibited the growth of WiDr cells compared to Oldenlandia diffusa extract and anti-cancer drugs alone. Conclusions : Oldenlandia diffusa extract has an apoptotic role in human colorectal cancer cells and a potential role in developing therapeutic agents against colorectal cancer.
Lee, Soojin,Shim, Ji Hwan,Gim, Huijin,Park, Hyun Soo,Kim, Byung Joo KOREAN PHARMACOPUNCTURE INSTITUTE 2016 Journal of pharmacopuncture Vol.19 No.1
Objectives: Oldenlandia diffusa is traditionally used to relieve the symptoms of and to treat various diseases, but its anti-cancer activity has not been well studied. In the present study, the authors investigated the anti-cancer effects of an ethanol extract of Oldenlandia diffusa (EOD) on HT-29 human adenocarcinoma cells. Methods: Cells were treated with different concentrations of an EOD, and cell death was assessed by using a 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay. Analyses of the sub G1 peak, the caspase-3 and -9 activities, and the mitochondrial membrane depolarizations were conducted to confirm cell death by apoptosis. Also, intracellular reactive oxygen species (ROS) generation was determined using carboxy-H2DCFDA (5-(and-6)-carboxy-20,70-dichlorodihydrofluorescein diacetate). Results: EOD inhibited the proliferation of HT-29 cells for 24 hours by $78.6%{\pm}8.1%$ at $50{\mu}g/mL$, $74.4%{\pm}4.6%$ at $100{\mu}g/mL$, $65.9%{\pm}5.2%$ at $200{\mu}g/mL$, $51.4%{\pm}6.2%$ at $300{\mu}g/mL$, and by $41.7%{\pm}8.9%$ at $400{\mu}g/mL$, and treatment for 72 hours reduced the proliferation at the corresponding concentrations by $43.3%{\pm}8.8%$, $24.3{\pm}5.1mV$, $13.5{\pm}3.2mV$, $6.5{\pm}2.3mV$, and by $2.6{\pm}2.3mV$. EOD increased the number of cells in the sub-G1 peak in a dose-dependent manner. The mitochondrial membrane depolarization was elevated by EOD. Also, caspase activities were dose-dependently elevated in the presence of EOD, and these activities were repressed by a pan-caspase inhibitor (zVAD-fmk). The ROS generation was significantly increased by EOD and N-acetyl-L-cysteine (NAC; a ROS scavenger) remarkably abolished EOD-induced cell death. In addition, a combination of sub-optimal doses of EOD and chemotherapeutic agents noticeably suppressed the growth of HT-29 cancer cells. Conclusion: These results indicate that EOD might be an effective chemotherapeutic for the treatment of human colorectal cancer.