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- 저자 : Heo Haejeong (검색결과 4 건)
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Heo Haejeong,Kim Jong-Hwan,Lim Hyun Jung,Kim Jeong-Hwan,Kim Miso,Koh Jaemoon,Im Joo-Young,Kim Bo-Kyung,Won Misun,Park Ji-Hwan,Shin Yang-Ji,윤미란,Cho Byoung Chul,Kim Yong Sung,Kim Seon-Young,김미랑 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
Acquired resistance to inhibitors of anaplastic lymphoma kinase (ALK) is a major clinical challenge for ALK fusion-positive non-small-cell lung cancer (NSCLC). In the absence of secondary ALK mutations, epigenetic reprogramming is one of the main mechanisms of drug resistance, as it leads to phenotype switching that occurs during the epithelial-to-mesenchymal transition (EMT). Although drug-induced epigenetic reprogramming is believed to alter the sensitivity of cancer cells to anticancer treatments, there is still much to learn about overcoming drug resistance. In this study, we used an in vitro model of ceritinib-resistant NSCLC and employed genome-wide DNA methylation analysis in combination with single-cell (sc) RNA-seq to identify cytidine deaminase (CDA), a pyrimidine salvage pathway enzyme, as a candidate drug target. CDA was hypomethylated and upregulated in ceritinib-resistant cells. CDA-overexpressing cells were rarely but definitively detected in the naïve cell population by scRNA-seq, and their abundance was increased in the acquired-resistance population. Knockdown of CDA had antiproliferative effects on resistant cells and reversed the EMT phenotype. Treatment with epigenome-related nucleosides such as 5-formyl-2′-deoxycytidine selectively ablated CDA-overexpressing resistant cells via accumulation of DNA damage. Collectively, our data suggest that targeting CDA metabolism using epigenome-related nucleosides represents a potential new therapeutic strategy for overcoming ALK inhibitor resistance in NSCLC.
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Epigenetic Activation of Tensin 4 Promotes Gastric Cancer Progression
Mirang Kim,Haejeong Heo,Hee-Jin Kim,Keeok Haam,Hyun Ahm Sohn,Yang-Ji Shin,Hanyong Go,Hyo-Jung Jung,Jong-Hwan Kim,Sang-Il Lee,Kyu-Sang Song,Min-Ju Kim,Haeseung Lee,Eun-Soo Kwon,Seon-Young Kim,Yong Sung 한국분자세포생물학회 2023 Molecules and cells Vol.46 No.5
Gastric cancer (GC) is a complex disease influenced by multiple genetic and epigenetic factors. Chronic inflammation caused by Helicobacter pylori infection and dietary risk factors can result in the accumulation of aberrant DNA methylation in gastric mucosa, which promotes GC development. Tensin 4 (TNS4), a member of the Tensin family of proteins, is localized to focal adhesion sites, which connect the extracellular matrix and cytoskeletal network. We identified upregulation of TNS4 in GC using quantitative reverse transcription PCR with 174 paired samples of GC tumors and adjacent normal tissues. Transcriptional activation of TNS4 occurred even during the early stage of tumor development. TNS4 depletion in GC cell lines that expressed high to moderate levels of TNS4, i.e., SNU-601, KATO III, and MKN74, reduced cell proliferation and migration, whereas ectopic expression of TNS4 in those lines that expressed lower levels of TNS4, i.e., SNU-638, MKN1, and MKN45 increased colony formation and cell migration. The promoter region of TNS4 was hypomethylated in GC cell lines that showed upregulation of TNS4. We also found a significant negative correlation between TNS4 expression and CpG methylation in 250 GC tumors based on The Cancer Genome Atlas (TCGA) data. This study elucidates the epigenetic mechanism of TNS4 activation and functional roles of TNS4 in GC development and progression and suggests a possible approach for future GC treatments.
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Cho, Seung-Ju,Kim, Keun-Tae,Kim, Jong-Soo,Kwon, Ok-Seon,Go, Young-Hyun,Kang, Nam-Young,Heo, Haejeong,Kim, Mi-Rang,Han, Dong Wook,Moon, Sung-Hwan,Chang, Young-Tae,Cha, Hyuk-Jin Elsevier 2018 Biomaterials Vol.180 No.-
<P><B>Abstract</B></P> <P>Human and mouse embryonic stem cells (ESCs) differ in terms of their pluripotency status, i.e., naïve vs. primed. This affects various biological properties and leads to several technical hurdles for future clinical applications, such as difficulties in chimera formation, single-cell passaging, and gene editing. In terms of generating functional human tissues and organs via mammalian interspecies chimerism, a fluorescent chemical probe that specifically labels naïve ESCs would help to isolate these cells and monitor their conversion. This study demonstrates that the fluorescent chemical probe compound of designation yellow 9 (CDy9) selectively stains naïve, but not primed, mouse ESCs (mESCs). CDy9 entered cells via Slc13a5, a highly expressed membrane transporter in naïve mESCs. Fluorescence-based cell sorting based on CDy9 staining successfully separated naïve mESCs from primed mESCs. Mice generated using CDy9<SUP>+</SUP> cells isolated during the conversion of mouse epiblast stem cells into naïve mESCs exhibited coat color chimerism. Furthermore, CDy9 specifically stained cells in the inner cell mass of mouse embryos. These findings suggest that CDy9 is a useful tool to isolate functional naïve mESCs.</P>
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Seon-Kyu Kim,Seon-Young Kim,Chan Wook Kim,Seon Ae Roh,하예진,Jong Lyul Lee,Haejeong Heo,Dong-Hyung Cho,이주석,Yong Sung Kim,Jin Cheon Kim 생화학분자생물학회 2019 Experimental and molecular medicine Vol.51 No.-
Approximately half of colorectal cancer (CRC) patients experience disease recurrence and metastasis, and theseindividuals frequently fail to respond to treatment due to their clinical and biological diversity. Here, we aimed toidentify a prognostic signature consisting of a small gene group for precisely predicting CRC heterogeneity. Weperformed transcriptomic profiling using RNA-seq data generated from the primary tissue samples of 130 CRCpatients. A prognostic index (PI) based on recurrence-associated genes was developed and validated in two largerindependent CRC patient cohorts (n = 795). The association between the PI and prognosis of CRC patients wasevaluated using Kaplan–Meier plots, log-rank tests, a Cox regression analysis and a RT-PCR analysis. Transcriptomicprofiling in 130 CRC patients identified two distinct subtypes associated with systemic recurrence. Pathwayenrichment and RT-PCR analyses revealed an eleven gene signature incorporated into the PI system, which was asignificant prognostic indicator of CRC. Multivariate and subset analyses showed that PI was an independent risk factor(HR = 1.812, 95% CI = 1.342–2.448, P < 0.001) with predictive value to identify low-risk stage II patients who respondedthe worst to adjuvant chemotherapy. Finally, a comparative analysis with previously reported Consensus MolecularSubgroup (CMS), high-risk patients classified by the PI revealed a distinct molecular property similar to CMS4,associated with a poor prognosis. This novel PI predictor based on an eleven gene signature likely represents asurrogate diagnostic tool for identifying high-risk CRC patients and for predicting the worst responding patients foradjuvant chemotherapy.
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