The biology of SCUBE

Lin, Yuh‐Charn; Sahoo, Binay K.; Gau, Susan Shur-Fen; Yang, Ruey‐Bing

doi:10.1186/s12929-023-00925-3

Cited by 4 publications

(1 citation statement)

References 211 publications

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“…All of these genes were downregulated, which raises the interesting possibility of defects in membrane polarization of KI ECs. Furthermore, other genes that are downregulated, specifically those involved in lipid metabolism such as Lrat, Dpep1, and Scube2, may lead to additional modifications to the membranes caused by the Y 685 F-VE-cadherin mutation (50, 51, 52). Further studies are needed to better understand the impact of this single mutation on the expression and function of transmembrane proteins in endothelial cells and vascular dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Efficient fine-tuning of endothelial gene expression by a single Tyrosine to Phenylalanine point mutation in theVE-cadheringene

Garnier,

Jeanneret,

Durand

et al. 2024

Preprint

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We aimed at understanding whether the site Y685 of VE-cadherin triggers epigenetic programming in vivo. Using our knock-in mice carrying the Y685F VE-cadherin mutation, RNA sequencing from lung ECs identified 884 differentially expressed genes (DEGs) involved in cell-cell adhesion, vascular development, and angiogenesis. Analysis of the VEGF/VEGFR2 signaling pathway shows a significant decrease in the expression of pY1173VEGFR2 whereas VEGF remains constant, this was consistent with impaired migration, proliferation and protrusive properties of ECs in vitro. Co-immunoprecipitation experiments showed that c-Src and Y685F VE-cadherin association which was enhanced in KI compared to WT, resulting in increased in Y685F-VE-cadherin phosphorylation at site Y731. As a consequence, its partner b-catenin translocates to the nucleus. Using CHIPS assay we demonstrate that FOXF1 binds to the s1pr1 promoter, leading to increased expression of the S1PR1, a process associated with increased vessel wall thickness and reduced fibrosis in the lung vasculature in vivo. Overall, our findings provide a novel transcriptomic profile triggered by Y685F-VE-cadherin ECs for potential insights into therapeutic targets to envisage normalisation of the tumor vasculature.

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Section: Discussionmentioning

confidence: 99%

Efficient fine-tuning of endothelial gene expression by a single Tyrosine to Phenylalanine point mutation in theVE-cadheringene

Garnier,

Jeanneret,

Durand

et al. 2024

Preprint

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SCUBE3 Exerts a Tumor-Promoting Effect in Tongue Squamous Cell Carcinoma by Promoting CEBPA Binding to the CCL2 Promoter

Zhu,

Ma,

Wang

et al. 2024

Molecular Cancer Research

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Tongue squamous cell carcinoma (TSCC) is the main pathological subtype of oral cancer, and the current therapeutic effect is far from satisfactory. The signal peptide-CUB-EGF domain-containing protein 3 (SCUBE3) has been shown to be a tumor-promoting factor in several malignancies. However, little is known about the role of SCUBE3 in TSCC. In this study, we identified that SCUBE3 was highly expressed in TSCC. Clinically, high expression of SCUBE3 was positively associated with tumor stage and T stage of TSCC. Functionally, SCUBE3 silence remarkably restrained cell proliferation, migration and invasion, induced apoptosis as well as cell cycle arrest in G2 phase, and weakened the tumorigenicity of TSCC cells in vivo. Mechanistically, SCUBE3 promoted the direct binding of CCAAT enhancer binding protein alpha (CEBPA) to C-C motif chemokine ligand 2 (CCL2) promoter in TSCC cells. Interestingly, CCL2 overexpression partially reversed the inhibitory effect of SCUBE3 deficiency on TSCC cell viability and migration. Moreover, signal transducer and activator of transcription 3 (STAT3) signaling contributed to CCL2-mediated phenotypes in TSCC cells. Implications: our data revealed a tumor-promoting role for SCUBE3 in TSCC via the CEBPA/ CCL2/STAT3 axis, which provided new insight into novel potential therapeutic target for TSCC.

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Inflammation: Complexity and significance of cellular and molecular responses

Özdemir

2024

Journal of Acute Disease

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Inflammation is a multifaceted cellular and molecular response triggered by injury, infection, or various pathological conditions. Serving as a protective defense mechanism, the inflammatory response involves clinical signs like redness, swelling, pain, and increased body temperature. Immune cells, notably neutrophils and macrophages, play key roles in orchestrating this response. The delicate balance between proinflammatory and anti-inflammatory mediators, including cytokines and chemokines, regulates the inflammatory cascade. While acute inflammation is crucial for tissue repair, chronic inflammation may indicate an imbalance, contributing to conditions like autoimmune diseases. Understanding these mechanisms is vital for developing therapeutic strategies and managing chronic diseases.

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The biology of SCUBE

Cited by 4 publications

References 211 publications

Efficient fine-tuning of endothelial gene expression by a single Tyrosine to Phenylalanine point mutation in theVE-cadheringene

Efficient fine-tuning of endothelial gene expression by a single Tyrosine to Phenylalanine point mutation in theVE-cadheringene

SCUBE3 Exerts a Tumor-Promoting Effect in Tongue Squamous Cell Carcinoma by Promoting CEBPA Binding to the CCL2 Promoter

Inflammation: Complexity and significance of cellular and molecular responses

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