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Invited Mini Review : Implications of NQO1 in cancer therapy
( Eun Taex Oh ),( Heon Joo Park ) 생화학분자생물학회(구 한국생화학분자생물학회) 2015 BMB Reports Vol.48 No.11
NAD(P)H:quinone oxidoreductase (NQO1), an obligatory two-electron reductase, is a ubiquitous cytosolic enzyme that catalyzes the reduction of quinone substrates. The NQO1- mediated two-electron reduction of quinones can be either chemoprotection/detoxification or a chemotherapeutic response, depending on the target quinones. When toxic quinones are reduced by NQO1, they are conjugated with glutathione or glucuronic acid and excreted from the cells. Based on this protective effect of NQO1, the use of dietary compounds to induce the expression of NQO1 has emerged as a promising strategy for cancer prevention. On the other hand, NQO1-mediated two-electron reduction converts certain quinone compounds (such as mitomycin C, E09, RH1 and -lapachone) to cytotoxic agents, leading to cell death. It has been known that NQO1 is expressed at high levels in numerous human cancers, including breast, colon, cervix, lung, and pancreas, as compared with normal tissues. This implies that tumors can be preferentially damaged relative to normal tissue by cytotoxic quinone drugs. Importantly, NQO1 has been shown to stabilize many proteins, including p53 and p33ING1b, by inhibiting their proteasomal degradation. This review will summarize the biological roles of NQO1 in cancer, with emphasis on recent findings and the potential of NQO1 as a therapeutic target for the cancer therapy. [BMB Reports 2015; 48(11): 609-617]
Oh, Eun-Taex,Park, Moon-Taek,Choi, Bo-Hwa,Ro, Seonggu,Choi, Eun-Kyung,Jeong, Seong-Yun,Park, Heon Joo M. Nijhoff ; Kluwer Academic Publishers 2012 Investigational new drugs Vol.30 No.2
<P>Histone deacetylase (HDAC) plays an important role in cancer onset and progression. Therefore, inhibition of HDAC offers potential as an effective cancer treatment regimen. CG200745, (E)-N-1-(3-(dimethylamino)propyl)-N-8-hydroxy-2-((naphthalene-1-loxy)methyl)oct-2-enediamide, is a novel HDAC inhibitor presently undergoing a phase I clinical trial. Enhancement of p53 acetylation by HDAC inhibitors induces cell cycle arrest, differentiation, and apoptosis in cancer cells. The purpose of the present study was to investigate the role of p53 acetylation in the cancer cell death caused by CG200745. CG200745-induced clonogenic cell death was 2-fold greater in RKO cells expressing wild-type p53 than in p53-deficient RC10.1 cells. CG200745 treatment was also cytotoxic to PC-3 human prostate cancer cells, which express wild-type p53. CG200745 increased acetylation of p53 lysine residues K320, K373, and K382. CG200745 induced the accumulation of p53, promoted p53-dependent transactivation, and enhanced the expression of MDM2 and p21(Waf1/Cip1) proteins, which are encoded by p53 target genes. An examination of CG200745 effects on p53 acetylation using cells transfected with various p53 mutants showed that cells expressing p53 K382R mutants were significantly resistant to CG200745-induced clonogenic cell death compared with wild-type p53 cells. Moreover, p53 transactivation in response to CG200745 was suppressed in all cells carrying mutant forms of p53, especially K382R. Taken together, these results suggest that acetylation of p53 at K382 plays an important role in CG200745-induced p53 transactivation and clonogenic cell death.</P>
Aurora-a contributes to radioresistance by increasing NF-kappaB DNA binding.
Oh, Eun-Taex,Byun, Mi-Sun,Lee, Hyemi,Park, Moon-Taek,Jue, Dae-Myung,Lee, Chang-Woo,Lim, Byung Uk,Park, Heon Joo Academic Press 2010 Radiation research Vol.174 No.3
<P>Abstract Aurora-A, a serine/threonine kinase that is overexpressed in certain human cancer cell lines, plays an important role in mitotic progression. Aurora-A has also been reported to be involved in the activation of nuclear factor kappa B (NF-kappaB). The purpose of the present study was to identify the role of Aurora-A in the radiation-induced activation pathway of NF-kappaB. Wild-type and Aurora-A knockdown (Aurora-A(KD)) HeLa cells were irradiated with 4 Gy of gamma rays and the EMSA, luciferase reporter gene assay and immunoblot analysis were performed. The siRNA-based gene knockdown and overexpression system was adopted to elucidate the role of Aurora-A in radiation-induced NF-kappaB pathway activation. The clonogenic survival study indicated that Aurora-A(KD) cells and the wild-type cells transfected with Aurora-A siRNA or RelA/p65 siRNA were more radiosensitive than the wild-type cells. In both the wild-type and Aurora-A(KD) cells, radiation caused IkappaB kinase-mediated phosphorylation, degradation of IkappaBalpha and phosphorylation of RelA/p65. The nuclear translocation of RelA/p65 was also similar in the wild-type and Aurora-A(KD) cells. However, RelA/p65-DNA binding was markedly suppressed in Aurora-A(KD) cells compared to that in wild-type cells. It was concluded that Aurora-A enhances the binding of NF-kappaB to DNA, thereby increasing the gene transcription by NF-kappaB and decreasing the radiosensitivity of the cells.</P>
Oh, Eun-Taex,So, Jae-Seong,Kim, Byung-Hyuk,Kim, Jong-Sul,Koh, Sung-Cheol The Microbiological Society of Korea 2004 The journal of microbiology Vol.42 No.3
Sphingomonas chlorophenolica ATCC39723 was successfully labeled with the gfp (green fluorescent protein) gene inserted into the pcpB gene by homologous recombination. As the gfp recombinant was easily distinguished from other indigenous organisms, the population of gfp recombinant was monitored after being released into the soil microcosms. Their population density dropped from 10$\^$8/ to 10$\^$6/ (cfu/$m\ell$) in the non-sterilized soil microcosms during the first 6 days. Moreover, the gfp recombinant was not detected even at lower dilution rates after a certain time period. The recombinant, however, survived for at least 28 days in the sterilized soil microcosms. Although the gfp recombinant did not degrade pentachlorophenol (PCP), this experiment showed the possibility of using gfp as a monitoring reporter system for S. chlorophenolica ATCC39723 and potentially other species of Sphingomonas.
Mehta, Pramod Kumar,Oh, Eun-Taex,Park, Heon Joo,Lee, Keun-Hyeung Elsevier 2018 Sensors and actuators. B Chemical Vol.256 No.-
<P><B>Abstract</B></P> <P>Ratiometric detection of Cu<SUP>+</SUP> in aqueous buffered solutions and live cells is highly recomended. We synthesized a fluorescent probe (<B>1)</B> based on the peptide receptor to mimic the binding site of the metalloprotein (CusF) for Cu<SUP>+</SUP>. <B>1</B> sensitively and selectively detected Cu<SUP>+</SUP> among various biological relevant metal ions in aqueous solutions at physiological pH through a ratiometric response. Job’s plot analysis indicated that <B>1</B> formed a 2:1 complex with Cu<SUP>+</SUP> and the binding affinity of <B>1</B> for Cu<SUP>+</SUP> was measured to be 5.73×10<SUP>−21</SUP> M<SUP>2</SUP> from a competition experiment with bathocuproine disulfonate. The probe showed significant ratiometric responses to Cu<SUP>+</SUP> over a wide range of pH (6.5∼10.5). The binding mode study showed that the imidazole and indole groups of the peptide receptor played a critical role in the tight binding to Cu<SUP>+</SUP>. <B>1</B> penetrated successfully in living A549 cells and detected intracellular Cu<SUP>+</SUP> ions in Golgi apparatus through ratiometric response. Giving the recent growing interests in fluorescent imaging of Cu<SUP>+</SUP>, the development of a fluorescent ratiometric probe (<B>1)</B> based on the peptide receptor to mimic the binding site of the metalloprotein for Cu<SUP>+</SUP> will provide a potential tool for detection of intracellular metal ions in live cells.</P> <P><B>Highlights</B></P> <P> <UL> <LI> The fluorescent peptidyl probe for Cu(I) was easily synthesized in high yield (75%). </LI> <LI> Highly sensitive and selective response to Cu(I) among various biological relevant metal ions. </LI> <LI> Ratiometric response to Cu(I) and the intensity ratio (I<SUB>472</SUB>/I<SUB>396</SUB>) at 472 and 396nm increased by about 130 fold. </LI> <LI> Cell penetration and ratiometric detection of intracellular Cu(I) in the Golgi apparatus in live cells. </LI> </UL> </P>
Cervicovaginal fluid hyaluronan in high risk of preterm birth: preliminary study
( Soo Ran Choi ),( Eun-taex Oh ) 대한산부인과학회 2022 대한산부인과학회 학술대회 Vol.108 No.-
Objective: Hyaluronan(HA) is a nonsulfated glycosaminoglycan and is synthesized at cervical epithelium and stroma and released into the cervicovaginal fluid. During pregnancy HA level increase in the cervix. HA depletion in the cervix resulted strikingly increased preterm birth rates in a mouse model. The objective of study was to identify the change of cervicovaginal fluid HA level in women with high risk of preterm birth. Methods: Cervicovaginal fluids were prospectively collected in 9 pregnant women at 16-27 weeks of gestation. HA and gelatinase were quantified by an enzyme-linked immunosorbent assay (ELISA) and Western blot. Results: In women who has short cervical length, cervicovaginal fluid HA levels were decreased than those of normal cervical length. The levels of cervicovaginal fluid gelatinase were increased in women with high risk of preterm birth. Conclusion: Decreased level of cervicovaginal fluid HA along with increased level of gelatinase may associated with preterm birth in who have short cervical length.