https://scholar.dgist.ac.kr/handle/20.500.11750/329 2026-05-21T20:13:45Z https://scholar.dgist.ac.kr/handle/20.500.11750/60354 Title: Histone mark remodeling in cancer: an enhancer-centered perspective Author(s): Park, Jiyoon; Jeon, Jinha; Gim, Sujeong; Chung, Chan Abstract: Epigenetic deregulation is a defining feature of cancer, and histone modification remodeling plays a central role in reshaping malignant transcriptional programs. Histone marks collectively organize chromatin states that govern enhancer activity, promoter competence, and stability of repressive domains. Across diverse tumor types, redistribution of active and repressive histone modifications reconfigures regulatory landscapes that sustain oncogenic amplification, lineage plasticity, and adaptive resistance. In this review, we examine histone mark remodeling in cancer through an enhancer-centered perspective. We discuss how the gain of H3K27ac-marked enhancers, super-enhancer formation, the erosion of lineage-restrictive regulatory elements, and the redistribution of repressive marks cooperate to reorganize transcriptional circuitry. We further outline the convergent mechanisms driving these alterations, including mutations in chromatin regulators, signal-dependent modulation of epigenetic enzymes, metabolic influences on chromatin state, and changes in three-dimensional genome architecture. The functional consequences of histone mark reprogramming, ranging from cell state transitions and tumor heterogeneity to transcriptional dependency and therapy-associated chromatin adaptation, are considered in the context of tumor evolution. Finally, we highlight emerging single-cell, spatial, and integrative multi-omics approaches that enable systems-level interpretation of chromatin landscapes and identification of context-specific vulnerabilities. By framing histone modification dynamics in terms of enhancer reconfiguration, this review provides a mechanistic and translational perspective on how chromatin remodeling sustains malignant identity and offers opportunities for therapeutic intervention. https://scholar.dgist.ac.kr/handle/20.500.11750/60353 Title: MLPH-mediated activation of dermal papilla IGF-1 signaling drives human hair shaft elongation and anagen induction Author(s): Kwack, Mi Hee; Kang, Eunho; Kim, Jewoo; Ji, Youngheum; Ju, Hyeonchang; Lee, Chang-Hun; Sung, Young Kwan; Kim, So Yeon; Moon, Cheil Abstract: Introduction Hair loss (alopecia) is a multifactorial disorder that often causes distress. Approved therapies such as minoxidil and finasteride act indirectly and do not specifically target hair follicle (HF) cells. Erythropoietin (EPO), however, has been shown to activate dermal papilla (DP) cells via the erythropoietin receptor (EPOR), suggesting a potential role in hair follicle regeneration and hair growth. Objectives This study aimed to develop and validate Helix C-1–based EPO-derived peptides that activate DP cells and increase IGF-1 expression, while not inducing overt systemic erythropoietic effects (e.g., increases in red blood cell counts, reticulocytes, hemoglobin, or hematocrit) under the tested experimental conditions. Methods Peptides derived from the Helix C-1 region of EPO were synthesized and characterized by EPOR-binding affinity, CD spectroscopy, and ERK/AKT activation. In vitro, DP-cell metabolic activity, proliferation, and IGF-1 secretion were assessed. Ex vivo efficacy was evaluated by hair shaft elongation in hair follicle organ culture, and in vivo efficacy was tested in a murine depilation-induced anagen model with concurrent hematologic assessment to exclude erythropoiesis-related effects. Results The peptides increased DP-cell metabolic activity and proliferation, reduced oxidative stress, and enhanced IGF-1 production via EPOR-mediated ERK/AKT activation. They promoted hair shaft elongation ex vivo and promoted anagen entry in mice without significant changes in standard hematologic parameters under the tested dosing regimen. Conclusion These findings support the conclusion that MLPH promotes hair growth via an EPOR-linked, IGF-1–dependent mechanism in DP cells. Future pharmacokinetic and disease-model studies are warranted to evaluate its translational potential. © 2026 The Authors. 2026-02-28T15:00:00Z https://scholar.dgist.ac.kr/handle/20.500.11750/60337 Title: Proteomics and phosphoproteomics of human colorectal cancer cells lacking a specific kinase activity reveal kinase-specific compensatory responses Author(s): Han, Bitnara; Lim, Hyun Ji; Kim, Su-Jung; Shin, Jaejin; Kim, Hyeong Hwan; Kim, Kyun-Hwan; Nam, Chang-Hoon; Kim, Kwang Pyo Abstract: Cell signaling regulates cell proliferation, survival, and migration, and abnormal kinase activity is often implicated in cancer. Although kinases are key targets for anticancer therapy, drug-induced compensatory signaling and pathway rewiring often drive acquired resistance. These compensatory responses enable tumor cells to maintain proliferation and survival, contributing to acquired drug resistance. In this study, we investigated adaptive responses following the knockout of four specific kinase genes, ERK2, PLK1, PIK3CA, and PAK4, using HCT-116, a human colorectal cancer cell line. Using CRISPR-Cas9, we generated individual knockout cell lines and conducted quantitative proteomic and phosphoproteomic profiling using isobaric tagging and tandem mass tag (TMTs) to evaluate alterations in the signaling landscape. Our integrated analysis quantified 7,531 proteins and 10,877 phosphopeptides, revealing kinase-specific patterns of compensatory signaling. ERK2 knockout was associated with activation of MAPK- and PI3K/AKT-related kinases, whereas PIK3CA knockout induced extensive proteomic remodeling and engagement of pro-survival phosphorylation programs, illustrating distinct modes of signaling network rewiring. Integration of kinase-substrate enrichment analysis (KSEA) with global proteomic data revealed that adaptive kinase activity was largely uncoupled from protein abundance and uncovered a synthetic lethal interaction between ERK2 loss and RPS6KB1 inhibition. Collectively, these findings elucidate how targeted kinase loss drives homeostatic signaling networks in cancer cells. By systemically characterizing cellular-level signaling changes and contextualizing them within known kinase pathways, our results provide insights into synthetic lethality and identify potential therapeutic targets to counteract adaptive resistance to kinase inhibitors. 2026-01-31T15:00:00Z https://scholar.dgist.ac.kr/handle/20.500.11750/60326 Title: 사람 질 오가노이드의 제조방법 및 이의 용도 Author(s): 명지현; 정영태 Abstract: 사람 질 오가노이드의 제조방법 및 이의 용도에 관한 것으로, 사람 질의 중층편평상피(stratified squamous epithelium)을 재현하는 사람 질 오가노이드 제조용 배지 및 제조 방법을 제공하며, 이를 활용하여 사람 질 오가노이드의 장기 계대배양을 가능케 하며, 약물 처리 및 질 줄기세포 특성 연구 플랫폼으로 활용할 수 있다.