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Yoon-Jin Lee,Yong-Jin Lee,Ihl-Sung Park,Jun-Hwan Song,Myung-Ho Oh,Hae-Seon Nam,Moon-Kyun Cho,Kee-Min Woo,Sang-Han Le 대한독성 유전단백체 학회 2015 Molecular & cellular toxicology Vol.11 No.3
Quercetin, a naturally occurring flavonoid, has been heralded as a promising chemopreventive agent. This study was undertaken to probe the molecular mechanisms underlying the anti-cancer activity of quercetin in malignant mesothelioma (MM) cells. Quercetin at low doses elicited apoptotic cell death on MM MSTO-211H cells, as signified by pyknotic and fragmented nuclei, increased annexin V binding, and increased proportion of cells with hypodiploid DNA. Preceding these changes, quercetin induced up-regulation of p53 at both mRNA and protein levels without altering its ubiquitination, and increased caspase-3/7 activity with the resultant cleavages of procaspase-3 and PARP. Analyses of nuclear p53 level, p53 reporter gene, and RT-PCR toward p53-regulated genes demonstrated that induced p53 is transcriptionally active. The proportion of cells at sub-G0/G1 peak and G2/M phase increased in a quercetin concentration-dependent fashion, which were blocked by the pan-caspase inhibitor Z-VAD. Additionally, quercetin and gemcitabine produced a significant synergistic effect on inhibiting MSTO- 211H cell growth. Given that quercetin induced preferential p53-upregulating, growth-inhibiting, and apoptosis-activating effects on MM cells, the use of quercetin may be a potential therapeutic strategy for enhancing anti-cancer efficacy of existing chemotherapy in MM.
Reflection on Kinetic Models to the Chlorine Disinfection for Drinking Water Production
Yoon-jinLee,Sang-hoNam 한국미생물학회 2002 The journal of microbiology Vol.40 No.2
Experiments for the characterization of inactivation were performed in a series of batch processes with the total coliform used as a general indicator organism based on the chlorine residuals as a disinfectant. The water samples were taken from the outlet of a settling basin in a conventional surface water treatment system that is provided with the raw water drawn from the mid-stream of the Han River. The inactivation of total coliform was experimentally analyzed for the dose of disinfectant, contact time, filtration and mixing intensity. The curves obtained from a series of batch processes were shaped with a general tailing-off and biphasic mode of inactivation, i.e. a sharp loss of bacterial viability within 15 min followed by an extended phase. In order to observe the effect of carry-over suspended solids on chlorine consumption and disinfection efficiency, the water samples were filtered, prior to inoculation with coliforms, with membranes of both 2.5 mm and 11.0 mm pore size, and with a sand filter of 1.0 mm in effective size and of 1.4 in uniformity coefficient. As far as the disinfection efficiency is concerned, there were no significant differences. The parameters estimated by the models of Chick-Watson, Hom and Selleck from our experimental data obtained within 120 min are: log(N/N0)=-0.16CT with n=1, log(N/N0)=-0.71C0.87T with n1 for the Chick-Watson model, log (N/N0)=-1.87C0.47T0.36 for the Hom model, log (N/N0)=-2.13log (1+CT/0.11) for the Selleck model. It is notable that among the models reviewed with regard to the experimental data obtained, the Selleck model appeared to most closely resemble the total coliform survival curve.
The Role of Heat Shock Protein 25 in Radiation Resistance
Yoon-Jin Lee,Su-Jae Lee,Sangwoo Bae,Yun-Sil Lee 한국환경성돌연변이발암원학회 2005 한국환경성돌연변이·발암원학회지 Vol.25 No.2
Overexpression of HSP25 delayed cell growth, increased the level of p21^(waf), reduced the levels of cyclin D1, cylcin A and cdc2, and induced radioresistance in L929 cells. We demonstrated that extracellular regulated kinase (ERK) and MAP kinase/ERK kinase (MEK) expressions as well as their activation (phospho-forms) were inhibited by hsp25 overexpression. To confirm the relationship between ERK1/2 and hsp25-mediated radioresistance, ERK1 or ERK2 cDNA was transiently transfected into the hsp25 overexpressed cells and their radioresistance was examined. HSP25-mediated radioresistance was abolished by overexpression of ERK2, but not by overexpression of ERK1. Alteration of cell cycle distribution and cell cycle related protein expressions (cyclin D, cyclin A and cdc2) by hsp25 overexpression were also recovered by ERK2 cDNA transfection. Increase in Bcl-2 protein by hsp25 gene transfection was also reduced by subsequent ERK2 cDNA-transfection. In addition, HSP25 overexpression reduced reactive oxygen species (ROS) and increased expression of manganese superoxide dismutase (MnSOD) gene. Increased activation of NF-kB (IkB degradation) was also found in hsp25-overexpressed cells. Moreover, transfection of hsp25 antisense gene abrogated all the HSP25-mediated phenomena. To further elucidate the exact relationship between MnSOD induction and NF-kB activation, dominant negative I-kBα (I-kBα-DN) construction was transfected to HSP25 overexpressed cells. I-kBα-DN inhibited HSP25 mediated MnSOD gene expression. In addition, HSP25 mediated radioresistance was blocked by I-kBα-DN transfection. Blockage of MnSOD with antisense oligonucleotides in HSP25 overexpressed cells, prevented apoptosis and returned the ERK1/2 activation to the control level. From the above results, we suggest for the first time that reduced oxidative damage by HSP25 was due to MnSOD-mediated downregulation of ERK1/2.
( Yoon Jin Lee ),( Sun Bum Kwon ),( Chul Han Kim ),( Hyun Deuk Cho ),( Hae Seon Nam ),( Sang Han Lee ),( Mi Woo Lee ),( Doo Hyun Nam ),( Chang Yong Choi ),( Moon Kyun Cho ) 대한피부과학회 2015 Annals of Dermatology Vol.27 No.5
Background: Reactive oxygen species (ROS) play an important role in the induction of apoptosis under pathological conditions. Recently, a significant increase in ROS production and disrupted apoptosis mechanisms in keloids have been reported. Nuclear factor erythroid 2-related factor 2 (Nrf2) represents one of the most important cellular defense mechanisms against oxidative stress and is implicated in the regulation of apoptosis. Recently, it has been reported that Nrf2 upregulates Bcl-2, an anti-apoptotic protein. Objective: To compare Nrf2 protein expression in normal skin tissues to keloid tissues. Methods: ROS generation in keloid tissues was evaluated with OxyBlot analysis. Western blotting and/or immunohistochemical staining approaches were used to study expression of Nrf2 or Bcl-2 in keloid and normal skin tissues. Cellular fractionation was performed to examine subcellular distribution of Nrf2. Transfection of fibroblasts with Nrf2-specific small interfering RNA (siRNA) was conducted to understand the relationship between Nrf2 expression and apoptosis induction. Results: Protein oxidation, a marker of oxidative stress, is increased in keloid tissues. Western blot analysis clearly showed that Nrf2 and Bcl-2 are downregulated in keloid tissues. Immunohistochemical staining of Nrf2 confirmed the results of the western blot analysis. Transfection of fibroblasts with the Nrf2-specific siRNA results in increased apoptosis and decreased cell viability. Conclusion: Collectively, our data indicate that Nrf2 expression is downregulated in keloid tissues, and that Nrf2 is involved in the development of apoptosis in Nrf2 siRNA-transfected fibroblasts. We propose that a defective antioxidant system and apoptotic dysregulation may participate in keloid pathogenesis. (Ann Dermatol 27(5) 507∼516, 2015)
( Yoon Jin Lee ),( Yong Jin Lee ),( Sang Han Lee ) 생화학분자생물학회(구 한국생화학분자생물학회) 2015 BMB Reports Vol.48 No.3
We previously demonstrated that resveratrol and clofarabine elicited a marked cytotoxicity on malignant mesothelioma (MM) MSTO-211H cells but not on the corresponding normal mesothelial MeT-5A cells. Little is known of the possible molecules that could be used to predict preferential chemosensitivity on MSTO-211H cells. Resveratrol and clofarabine induced down-regulation of Mcl-1 protein level in MSTO- 211H cells. Treatment of cells with cycloheximide in the presence of proteasome inhibitor MG132 suggested that Mcl-1 protein levels were regulated at the post-translational step. The siRNA-based knockdown of Mcl-1 in MSTO-211H cells triggered more growth-inhibiting and apoptosis-inducing effects with the resultant cleavages of procaspase-3 and its substrate PARP, increased caspase-3/7 activity, and increased percentage of apoptotic propensities. However, the majority of the observed changes were not shown in MeT-5A cells. Collectively, these studies indicate that the preferential activation of caspase cascade in malignant cells might have important applications as a therapeutic target for MM.[BMB Reports 2015; 48(3): 166-171]
Overexpression of Nrf2 promotes colon cancer progression via ERK and AKT signaling pathways
Yoon Jin Lee,Woo Il Kim,Jin Ho Bae,Moon Kyun Cho,Sang Han Lee,Hae Seon Nam,In Ho Choi,Sung Woo Cho 대한외과학회 2020 Annals of Surgical Treatment and Research(ASRT) Vol.98 No.4
Purpose: We investigated the expression of Nrf2 in colorectal cancer and its correlation with clinicopathological characteristics as well as mechanisms and roles of Nrf2 expression including cell signaling pathway, survival, proliferation, and migration. Methods: Nrf2 expression was measured in 12 and 30 different colorectal cancer (CRC) tissues by western blot (WB) and immunohistochemistry (IHC), respectively. SW480 cells were used for cell proliferation and cell migration tests. The correlation between the expression of Nrf2 and clinicopathologic parameters were evaluated using the chi-square or Fisher exact test. Data are expressed as the mean ± standard deviation for 3 independent experiments. P < 0.05 was considered statistically significant. Results: Analysis of WB demonstrated that Nrf2 proteins were increased in CRC tissues, and decreased in normal tissues. IHC staining showed that the Nrf2 expression was elevated in CRC tissues, compared to matched normal tissues. When SW480 cells were suppressed with small interfering RNA of Nrf2, cell viability was inhibited, and cell apoptosis was increased. These results were found along with suppression of the phosphorylated form of extracellular signal-regulated kinase 1/2 and AKT. Conclusion: This study suggests that overexpression of Nrf2 may be related to carcinogenesis and progression of CRC.