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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>
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,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.
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>
Lee, Jeonghun,Oh, Eun-Taex,Choi, Min Hyeuk,Kim, Ha Gyeong,Park, Heon Joo,Kim, Chulhee The Royal Society of Chemistry 2018 New journal of chemistry Vol.42 No.15
<P>Cyclic peptide gatekeepers with a capability of on-off drug release triggered by stimuli-responsive conformational transformation on the surface of mesoporous silica nanocontainers (MSNs) has several advantages such as facile introduction of targeting ligand, high targeting selectivity, and low enzymatic degradation. In this report, a dual functional cyclic peptide gatekeeper containing A6 sequence on the surface of MSNs is prepared for active targeting of cancer cells with high CD44 expression along with the capability of triggered drug release. The entrapped DOX is released from the MSNs with A6-containing cyclic peptide gatekeepers <I>via</I> conformational transformation of the peptide triggered by intracellular glutathione of the cancer cells. Furthermore, the MSNs effectively induce apoptosis in MDA-MB-231 cells (with CD44 expression) while not in SK-BR-3 cells (without CD44 expression).</P>
Lee, Jeonghun,Oh, Eun-Taex,Lee, Jinyoung,Kang, Taehyeong,Kim, Ha Gyeong,Kang, Hansol,Park, Heon Joo,Kim, Chulhee The Royal Society of Chemistry 2019 NEW JOURNAL OF CHEMISTRY Vol.43 No.3
<P>Adopting conformational conversion of a peptide as a trigger to control on-off gatekeeping on the surface of mesoporous silica nanoparticles has several advantages. Here, we designed a dual-functional cyclic peptide with an iRGD sequence as a stimulus-responsive on-off gatekeeper on the surface of mesoporous silica nanocontainers. The cyclic peptide gatekeeper with an intramolecular disulfide bond between the two cysteine units at both terminals of the peptide sequence exhibited selective drug release triggered by stimulus-induced conformational conversion. Furthermore, the iRGD sequence of the cyclic peptide gatekeeper enhanced the intracellular uptake and therapeutic efficacy of the nanoparticles by specifically binding with NRP-1 receptor on the surface of target cancer cells.</P>
Lee, Jeonghun,Oh, Eun-Taex,Song, Jaehun,Kim, Ha Gyeong,Park, Heon Joo,Kim, Chulhee Wiley-VCH Verlag GmbH & Co. KGaA 2017 Chemistry - An Asian Journal Vol. No.
<P>alpha(v)beta(3) Integrin is upregulated on many cancer cells. We designed a dual functional cyclic peptide gatekeeper with a capability of stimuli-responsive conformational transformation which could serve as a selective cell-targeting on-off gatekeeper for mesoporous nanocarriers. The advantage of employing the motif of stimuli-induced conformational transformation of cyclic peptides is that they could be utilized not only as an on-off gatekeeper for the triggered release of cargo drugs but also as a targeting ligand of the carriers to desired cells with their respective binding receptors. The peptide gatekeepers on the surface of nanocarriers exhibited on-off gatekeeping via conformational transformation triggered by intracellular glutathione levels of the cancer cells. The cyclic RGD sequence of the peptide gatekeepers enhanced the intracellular uptake into tumor cells (A549) and the therapeutic efficacy of the nanocarrier.</P>