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3 results on '"Jiahui Cao"'

1. USP24 promotes autophagy-dependent ferroptosis in hepatocellular carcinoma by reducing the K48-linked ubiquitination of Beclin1

Author

Jiahui Cao, Shitao Wu, Senfeng Zhao, Libo Wang, Yahui Wu, Liming Song, Chenguang Sun, Yin Liu, Zhipu Liu, Rongtao Zhu, Ruopeng Liang, Weijie Wang, and Yuling Sun

Subjects
Biology (General), QH301-705.5
Abstract

Abstract Ubiquitination is a post-translational modification (PTM), which is critical to maintain cell homeostasis. Ubiquitin-specific protease 24 (USP24) plays roles in various diseases, the mechanisms by which USP24 regulates hepatocellular carcinoma (HCC) remain poorly understood. In this study, USP24 is found to be significantly downregulated in HCC. Knocking down USP24 promotes HCC proliferation and migration, whereas USP24 overexpression inhibits HCC in vitro and in vivo. The endogenous interaction between USP24 and Beclin1 is confirmed. Mechanically, USP24 delays Beclin1 degradation by reducing its K48-linked ubiquitination, the effects of overexpressing USP24 on HCC proliferation can be partially reversed by silencing Beclin1. We find that increased autophagy is accompanied by ferroptosis in USP24 overexpressed HCC cells and USP24 increases the susceptibility of HCC to sorafenib. Collectively, this study highlights the critical role of USP24 in regulating autophagy-dependent ferroptosis by decreasing Beclin1 ubiquitination, suggesting that targeting USP24 may be a strategy for treating HCC.

Published
2024
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2. Polarized actin and VE-cadherin dynamics regulate junctional remodelling and cell migration during sprouting angiogenesis

Author

Jiahui Cao, Manuel Ehling, Sigrid März, Jochen Seebach, Katsiaryna Tarbashevich, Tomas Sixta, Mara E. Pitulescu, Ann-Cathrin Werner, Boris Flach, Eloi Montanez, Erez Raz, Ralf H. Adams, and Hans Schnittler

Subjects
Science
Abstract

The formation of new blood vessels requires both polarized cell migration and coordinated control of endothelial cell contacts. Here, Cao and colleagues describe at the sub-cellular level the cytoskeletal and cell junction dynamics regulating these processes upon VEGF-induced cell elongation.

Published
2017
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3. Polarized actin and VE-cadherin dynamics regulate junctional remodelling and cell migration during sprouting angiogenesis

Author

Mara E. Pitulescu, Boris Flach, Ann Cathrin Werner, Eloi Montanez, Jiahui Cao, Katsiaryna Tarbashevich, Ralf H. Adams, Hans Schnittler, Manuel Ehling, Jochen Seebach, Sigrid März, Tomáš Sixta, and Erez Raz

Subjects
0301 basic medicine, Vascular Endothelial Growth Factor A, Antígens CD, Angiogenesis, Physiology, General Physics and Astronomy, Cell junction, Microtubules, Cell Movement, Pseudopodia, Cytoskeleton, lcsh:Science, Multidisciplinary, Chemistry, Factor de creixement de l'endoteli vascular, Models, Cardiovascular, Cell Polarity, Cell migration, Cadherins, Metabolisme, Cell biology, rac GTP-Binding Proteins, CD antigens, Intercellular Junctions, Actin-Related Protein 3, Actin-Related Protein 2, Lamellipodium, Wiskott-Aldrich Syndrome Protein, Signal Transduction, Myosin Light Chains, Cèl·lules, Cells, Science, Notch signaling pathway, Neovascularization, Physiologic, Fisiologia, Vascular Remodeling, General Biochemistry, Genetics and Molecular Biology, Actin-Related Protein 2-3 Complex, Article, Adherens junction, 03 medical and health sciences, Vascular endothelial growth factors, Antigens, CD, Cell Adhesion, Human Umbilical Vein Endothelial Cells, Humans, Neovascularization, Sprouting angiogenesis, Endothelial Cells, General Chemistry, social sciences, Vascular Endothelial Growth Factor Receptor-2, Actins, Wiskott-Aldrich Syndrome Protein Family, Angiogènesi, 030104 developmental biology, Metabolism, lcsh:Q, Endothelium, Vascular, Cardiac Myosins
Abstract

VEGFR-2/Notch signalling regulates angiogenesis in part by driving the remodelling of endothelial cell junctions and by inducing cell migration. Here, we show that VEGF-induced polarized cell elongation increases cell perimeter and decreases the relative VE-cadherin concentration at junctions, triggering polarized formation of actin-driven junction-associated intermittent lamellipodia (JAIL) under control of the WASP/WAVE/ARP2/3 complex. JAIL allow formation of new VE-cadherin adhesion sites that are critical for cell migration and monolayer integrity. Whereas at the leading edge of the cell, large JAIL drive cell migration with supportive contraction, lateral junctions show small JAIL that allow relative cell movement. VEGFR-2 activation initiates cell elongation through dephosphorylation of junctional myosin light chain II, which leads to a local loss of tension to induce JAIL-mediated junctional remodelling. These events require both microtubules and polarized Rac activity. Together, we propose a model where polarized JAIL formation drives directed cell migration and junctional remodelling during sprouting angiogenesis., The formation of new blood vessels requires both polarized cell migration and coordinated control of endothelial cell contacts. Here, Cao and colleagues describe at the sub-cellular level the cytoskeletal and cell junction dynamics regulating these processes upon VEGF-induced cell elongation.

Published
2017

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