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Last update 08 May 2025

PCOLCE

Last update 08 May 2025

Basic Info

Synonyms

PCOLCE, PCPE, PCPE-1

+ [7]

Introduction

Binds to the C-terminal propeptide of type I procollagen and enhances procollagen C-proteinase activity. C-terminal processed part of PCPE (CT-PCPE) may have an metalloproteinase inhibitory activity.

Drugs associated with PCOLCE

Brefeldin A

Target

PCOLCE

Mechanism

PCOLCE inhibitors

Active Org.

Sylvester Comprehensive Cancer Center [+1]

Originator Org.

National Institute of Child Health & Human Development

Active Indication

Glioma

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

CN114903974

Patent Mining

Target

PCOLCE

Mechanism-

Active Org.

Mudanjiang Medical University

Originator Org.

Mudanjiang Medical University

Active Indication

Connective and Soft Tissue Neoplasms

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with PCOLCE

100 Translational Medicine associated with PCOLCE

0 Patents (Medical) associated with PCOLCE

1,035

Literatures (Medical) associated with PCOLCE

24 Apr 2025·Blood

17(R)-Resolvin D1 protects against sickle cell–related inflammatory cardiomyopathy in humanized mice

Article

Author: Ghigo, Alessandra ; Gremese, Elisa ; Brugnara, Carlo ; Iezzi, Manuela ; Riccardi, Veronica ; Recchiuti, Antonio ; Ceolan, Jacopo ; Mattoscio, Domenico ; Ceci, Martina ; Matte, Alessandro ; Federti, Enrica ; De Franceschi, Lucia ; Cozzolino, Flora ; Monti, Maria ; Tolosano, Emanuela ; Siciliano, Angela

AbstractCardiovascular disease has been recognized as the main cause of death in adults with sickle cell disease (SCD). Although the exact mechanism linking SCD to cardiomyopathy remains elusive, a possible role of subclinical acute transient myocardial ischemia during acute sickle cell–related vaso-occlusive crises (VOCs) has been suggested. We approached SCD cardiomyopathy by integrated omics using humanized SS mice exposed to hypoxia/reoxygenation (H/R; 10 hours hypoxia followed by 3 hours reoxygenation) stress, mimicking acute VOCs. In sickle cell (SS) mice exposed to H/R, a neutrophil-driven cardiac hypertrophic response is initiated by cardiac proinflammatory pathways, intersecting proteins and micro RNA involved in profibrotic signaling. This response may be facilitated by local unresolved inflammation. We then examined the effect of 17(R)-resolvin D1 (17R-RvD1), a member of the specialized proresolving lipid mediator superfamily, administration on H/R-activated profibrotic and proangiogenic pathways. In SS mice, we found that 17R-RvD1 (1) modulates miRNAome; (2) prevents the activation of NF-κB p65; (3) protects against the H/R-induced activation of both platelet derived growth factor receptor and transforming growth factor (TGF)-β1/Smad2-3 canonical pathways; (4) reduces the expression of hypoxia-inducible factor-dependent proangiogenic signaling; and (5) decreases the H/R-induced proapoptotic cell signature. The protective role of 17R-RvD1 against H/R-induced maladaptive heart remodeling was supported by the reduction of galectin-3, procollagen C-proteinase enhancer-1, and endothelin-1 expression and perivascular fibrosis in SS mice at 3 days after H/R stress compared with vehicle-treated SS animals. Collectively, our data support the novel role of unresolved inflammation in pathologic heart remodeling in SCD mice in response to H/R stress. Our study provides new evidence for protective effects of 17R-RvD1 against SCD-related cardiovascular disease.

01 Apr 2025·Biochemical Genetics

Integration of Single-Cell and Bulk RNA-seq Data to Identify the Cancer-Associated Fibroblast Subtypes and Risk Model in Glioma

Article

Author: Liu, Zhihui ; Wang, Nan ; Hu, Xueyan ; Gao, Xin ; Yan, Xiuwei ; Hu, Shaoshan ; Xu, Lei ; Dong, Jiawei ; Wang, Fang ; Jiang, Xiaoyan ; Zhao, Hongtao ; Zhang, Jiheng

Cancer-associated fibroblasts (CAFs) are an important component of the stroma. Studies showed that CAFs were pivotally in glioma progression which have long been considered a promising therapeutic target. Therefore, the identification of prognostic CAF markers might facilitate the development of novel diagnostic and therapeutic approaches. A total of 1333 glioma samples were obtained from the TCGA and CGGA datasets. The EPIC, MCP-counter, and xCell algorithms were used to evaluate the relative proportion of CAFs in glioma. CAF markers were identified by the single-cell RNA-seq datasets (GSE141383) from the Tumor Immune Single-Cell Hub database. Unsupervised consensus clustering was used to divide the glioma patients into different distinct subgroups. The least absolute shrinkage and selection operator regression model was utilized to establish a CAF-related signature (CRS). Finally, the prognostic CAF markers were further validated in clinical specimens by RT‒qPCR. Combined single-cell RNA-seq analysis and differential expression analysis of samples with high and low proportions of CAFs revealed 23 prognostic CAF markers. By using unsupervised consensus clustering, glioma patients were divided into two distinct subtypes. Subsequently, based on 18 differentially expressed prognostic CAF markers between the two CAF subtypes, we developed and validated a new CRS model (including PCOLCE, TIMP1, and CLIC1). The nomogram and calibration curves indicated that the CRS was an accurate prognostic marker for glioma. In addition, patients in the high-CRS score group had higher immune infiltration and tumor mutation burden levels. Moreover, the CRS score had the potential to predict the response to immune checkpoint blockade (ICB) therapy and chemotherapy. Finally, the expression profiles of three CAF markers were verified by RT‒qPCR. In general, our study classified glioma patients into distinct subgroups based on CAF markers, which will facilitate the development of individualized therapy. We also provided insights into the role of the CRS in predicting the response to ICB and chemotherapy in glioma patients.

01 Apr 2025·European Journal of Medicinal Chemistry

Synthesis and evaluation of piceatannol derivatives as novel arginase inhibitors with radical scavenging activity and their potential for collagen reduction in dermal fibroblasts

Article

Author: Harakat, Dominique ; Pudlo, Marc ; Sénéjoux, François ; Zedet, Andy ; Gaudillat, Quentin ; Cardey, Bruno ; Girard, Corine ; Tissot, Marion ; Marchisio, Luca ; Rolin, Gwenaël ; Muller, Jason

High arginase activity is associated with several pathological conditions, including TGF-β-induced fibrosis, by increasing levels of the proline precursor l-ornithine, thereby promoting collagen biosynthesis and increasing oxidative stress due to nitric oxide synthase (NOS) uncoupling. The natural piceatannol has been shown to have beneficial effects on collagen deposition, fibrosis and oxidative stress. In this study, we present an in-depth structure-activity relationship study on arginase I, which resulted in the thioamide derivative 12a with dual catechol rings that displays potent inhibitory activity with IC₅₀ values of 9 μM and 55 μM for bovine and human arginase I, respectively. Quantum chemical modelling suggested that the sulphur atom in the thioamide group plays a crucial role in binding affinity by forming a stable hydrogen bond within the active site of the enzyme. In addition, compound 12a demonstrated high radical scavenging activity and effectively normalised collagen and procollagen levels at 5 μM in an in vitro cell model of a dermal fibrosis.

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PCOLCE

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