Eunae You
Korea University · Medicine
About the Lab
Professor Eunae You's research lab focuses on the mechanobiology of cancer and fibrosis, particularly how mechanical cues in the extracellular matrix regulate cellular behavior through cytoskeletal dynamics and signaling pathways. The lab investigates the roles of microtubule acetylation, SPIN90, and mechanosensitive transcriptional regulators like YAP in fibroblast activation, myofibroblast differentiation, and tumor microenvironment remodeling. A central theme is the interplay between mechanical stiffness, post-translational modifications of tubulin, and growth factor signaling in disease progression. The lab also explores innate immune evasion mechanisms in cancer, especially in pancreatic ductal adenocarcinoma, through viral mimicry and repeat element regulation.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15Abstract Biomechanical remodeling of stroma by cancer-associated fibroblasts (CAF) in early stages of cancer is critical for cancer progression, and mechanical cues such as extracellular matrix stiffness control cell differentiation and malignant progression. However, the mechanism by which CAF activation occurs in low stiffness stroma in early stages of cancer is unclear. Here, we investigated the molecular mechanism underlying CAF regulation by SPIN90 and microtubule acetylation under conditio
Cell signals for growth factors depend on the mechanical properties of the extracellular matrix (ECM) surrounding the cells. Microtubule acetylation is involved in the transforming growth factor (TGF)-β-induced myofibroblast differentiation in the soft ECM. However, the mechanism of activation of α-tubulin acetyltransferase 1 (α-TAT1), a major α-tubulin acetyltransferase, in the soft ECM is not well defined. Here, we found that casein kinase 2 (CK2) is required for the TGF-β-induced activation o
Abstract Repeat element viral mimicry is a common feature in pancreatic ductal adenocarcinoma (PDAC) that requires mechanisms to manage this repeat “viral” load and attenuate innate immune responses. In this study, we show that the long interspersed nuclear element 1 (LINE-1) open reading frame 1 protein (ORF1p) in PDAC cells plays a role in shielding repeat RNAs from activating a pathogen recognition receptor–mediated antiviral response that is independent of retrotransposition. Suppression of
Safflower (Carthamus tinctorius L.) is a versatile oilseed crop valued for its adaptability, high oil quality, and antioxidant properties. This study investigates the influence of flower color (FC) on the phenotypic diversity of 172 safflower accessions, analyzing agronomic traits, metabolite profiles, and antioxidant capacities. Frequency distribution, effect size, principal component analysis (PCA), and network analysis were employed to elucidate trait associations and interrelationships. FC s
Alterations in mechanical properties in the extracellular matrix are modulated by myofibroblasts and are required for progressive fibrotic diseases. Recently, we reported that fibroblasts depleted of SPIN90 showed enhanced differentiation into myofibroblasts via increased acetylation of microtubules in the soft matrix; the mechanisms of the underlying signaling network, however, remain unclear. In this study, we determine the effect of depletion of SPIN90 on FAK/ROCK signaling modules. Transcrip
Abstract Myofibroblasts are the major cell type that are responsible for increase the mechanical stiffness in fibrotic tissues. It has well documented that the TGF-β/Smad axis is required for myofibroblast differentiation under the rigid substrate condition. However, the mechanism driving myofibroblast differentiation in soft substrates remains unknown. In this research, we demonstrated that interaction of yes-associated protein (YAP) and acetylated microtubule via dynein, a microtubule motor pr
Abstract Aberrant transcription of the repeat RNAs is a common feature in epithelial cancers including PDAC, but the function of these non-coding RNAs in cancer development is relatively unexplored. We have found that these repeat RNAs are sensed and replicate like retroviruses, and now have identified the ability of these viral-like elements to be transmitted from cancer cells through extracellular vesicles (EVs). PDAC-derived EVs applied to cancer-associated fibroblasts (CAFs) activates interf
BACKGROUND: Perilla frutescens is a widely cultivated annual crop in East Asia, valued for its oil-rich seeds and edible leaves. The seeds are abundant in functional compounds such as unsaturated fatty acids, polyphenols, and flavonoids, and oil-extraction by-products are used as protein-rich animal feed and organic fertilizer. Despite its economic and nutritional significance, the genetic basis underlying major seed traits in Perilla remains poorly understood. RESULTS: To investigate the geneti
<div>Abstract<p>Repeat element viral mimicry is a common feature in pancreatic ductal adenocarcinoma (PDAC) that requires mechanisms to manage this repeat “viral” load and attenuate innate immune responses. In this study, we show that the long interspersed nuclear element 1 (LINE-1) open reading frame 1 protein (ORF1p) in PDAC cells plays a role in shielding repeat RNAs from activating a pathogen recognition receptor–mediated antiviral response that is independent of retrotranspositi
<p>Figure S1 (Related to Fig. 1). Low expression of SPIN90 in cancer stroma and CAFs. Figure S2 (Related to Fig. 2). CAFs derived from Spin90-/- mice show increased activation. Figure S3 (Related to Fig. 3). Loss of SPIN90 induces CAF differentiation. Figure S4 (Related to Fig. 4). Recruitment of mDia2 to acetylated microtubules regulates CAF differentiation. Figure S5 (Related to Fig. 5). Acetylated α-tubulin enhances nuclear translocation of YAP on 0.5 kPa PAGs. Figure S6 (Related to Fig
Abstract Transcriptional profiling has defined PDAC into distinct classical epithelial (E) or quasi-mesenchymal (QM) subtypes, and these subtypes exist on a continuum of interconverting cell states. This epithelial to mesenchymal transition (EMT) plasticity is thought to be important for the metastatic dissemination and intrinsic resistance to chemotherapy. Our prior work identified TAK1 as an important driver of EMT in mouse circulating tumor cells, and we had identified a compound (5z)-7-oxoze
Abstract Aberrant expression of repeat elements displaying viral mimicry is a common feature found in both mouse models and human pancreatic ductal adenocarcinoma (PDAC). However, cancer cells must employ mechanisms to manage this "viral" repeat element load to avoid triggering innate immune responses. Here, we demonstrate that the long interspersed nuclear element 1 (LINE-1) ORF1 protein (ORF1p) in PDAC cells plays a role in shielding repeat RNAs from activating pathogen recognition receptor (P
Research Areas
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