Publications by authors named "Ye Eun Hwang"

Over the past few decades, microtubules have been targeted by various anticancer drugs, including paclitaxel and eribulin. Despite their promising effects, the development of drug resistance remains a challenge. We aimed to define a novel cell death mechanism that targets microtubules using eribulin and to assess its potential in overcoming eribulin resistance.

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Article Synopsis
  • Microtubule acetylation impacts actin filament dynamics by influencing signaling pathways, but the exact processes are still unclear.
  • Disruption of ATAT1 reduces microtubule acetylation, leading to lower RhoA levels, which are crucial for actin organization and stress fiber formation.
  • C/EBPβ is a key regulator of RhoA, and its fragment C/EBPβp27, formed by cathepsin L in ATAT1 knockout cells, inhibits RhoA expression, suggesting potential targets for breast cancer therapies.
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Excessive production and accumulation of amyloid-beta (Aβ) in the brain are one of the hallmarks of Alzheimer's disease (AD). Although oxidative stress is known to trigger and promote the progression of AD, the molecular relationship between oxidative stress and Aβ production is not yet fully understood. In this study, we demonstrate that microtubule acetylation induced by oxidative stress plays a critical role in Aβ production and secretion by altering the subcellular distribution of Aβ precursor protein (APP)-containing lysosomal vesicles.

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Matrix stiffness has been shown to play a critical role in cancer progression by influencing various cellular processes, including epidermal growth factor (EGF) signaling. However, the underlying molecular mechanisms are not fully understood. Here, we investigated the role of adaptor-related protein complex 1 subunit sigma 1 (AP1S1), a component of adaptor protein complex-1, in the regulation of EGF receptor (EGFR) intracellular trafficking during cancer cell progression.

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Article Synopsis
  • Small cell lung cancer (SCLC) is a highly aggressive cancer with few treatment options, where tumor cell plasticity and immune evasion complicate therapies.
  • The study highlights CRACD, a protein often inactive in SCLC, as a key regulator that influences tumor cell behavior, with its loss leading to enhanced neuroendocrine plasticity and reduced immune response.
  • Targeting EZH2, a protein involved in gene regulation, presents a potential treatment strategy by restoring MHC-I expression, which can improve immune surveillance in CRACD-negative SCLC patients.
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Silicon carbide (SiC) is a very promising carbide material with various applications such as electrochemical supercapacitors, photocatalysis, microwave absorption, field-effect transistors, and sensors. Due to its enticing advantages of high thermal stability, outstanding chemical stability, high thermal conductivity, and excellent mechanical behavior, it is used as a potential candidate in various fields such as supercapacitors, water-splitting, photocatalysis, biomedical, sensors, and so on. This review mainly describes the various synthesis techniques of nanostructured SiC (0D, 1D, 2D, and 3D) and its properties.

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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.

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Purpose: Spatiotemporal regulation of cell membrane dynamics is a major process that promotes cancer cell invasion by acting as a driving force for cell migration. Beta-Pix (βPix), a guanine nucleotide exchange factor for Rac1, has been reported to be involved in actin-mediated cellular processes, such as cell migration, by interacting with various proteins. As yet, however, the molecular mechanisms underlying βPix-mediated cancer cell invasion remain unclear.

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During aggressive cancer progression, cancer cells adapt to unique microenvironments by withstanding various cellular stresses, including endoplasmic reticulum (ER) stress. However, the mechanism whereby cancer cells overcome the ER stress to survive remains to be elucidated. Herein, we demonstrated that microtubule acetylation in cancer cells grown on a stiff matrix promotes cancer progression by preventing excessive ER stress.

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