Inhibition of the proliferation and acceleration of migration of vascular endothelial cells by increased cysteine-rich motor neuron 1

Nakashima, Yukiko; Morimoto, Mayuka; Toda, Ken‐ichi; Shinya, Tomohiro; Sato, Keizo; Takahashi, Satoru

doi:10.1016/j.bbrc.2015.04.118

Cited by 4 publications

(9 citation statements)

References 13 publications

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“…CRIM1 over-expression in HCE-S cells leads to reduced proliferation (Fig.6B) and a parallel increase in apoptosis (Fig.6D), as expected following the previous results where CRIM1 was shown having a protective role in pterygium formation, counteracting the UV-induced proliferation (Fig.4B). This is in accordance with the downregulation of vascular endothelial cell proliferation after transient CRIM1 overexpression 54 and with the increase in cardiomyocyte proliferation following CRIM1 silencing through miR-199a 55,56 . Since the same miR-199a was found upregulated in pterygium 90 , this could analogously increase cell proliferation in pterygium formation through CRIM1 silencing, counteracting the protective effects of CRIM1 overexpression.…”

Section: Discussionsupporting

confidence: 85%

“…CRIM1 is thus proposed as a VEGFA antagonist 60,73 , possibly resisting pterygium formation by preventing angiogenesis as it has been shown to prevent proliferation 54,55 . Proliferation in cardiomyocytes is reduced by CRIM1 upregulation following miR199a silencing 55,56 , the same miRNA which was found overexpressed in pterygium 90 .…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have elucidated the importance of CRIM1 expression in corneal and conjunctival development [50][51][52] and the same variant, H412P, was identified from another WES study on patients affected by Coloboma eye developmental disorder 53 . Moreover, CRIM1 revealed a role in cell proliferation [54][55][56] , adhesion and migration [57][58][59] , angiogenesis through VEGFA 60-62 and UV-related diseases 63,64 , the main processes involved in pterygium development 4 .…”

Section: Wes Analysis In a Northern Irish Family Affected By Pterygiumentioning

confidence: 99%

“…Since a decrease in proliferation was reported in vascular endothelial cells after transient CRIM1 overexpression 54 , an in vitro MTT proliferation assay was then performed in HCE-S cells transfected with CRIM1 wild type or H412P constructs (Fig.6B). Compared to mock transfected HCE-S cells, wild type CRIM1 overexpression had a relevant anti-proliferative effect, which was most significant at 72 hours post-transfection (absorbance 72-24 hours 0.60 ± 0.02 OD; p<0.01).…”

Section: Effects Of Wild Type and H412p Mutant Crim1 Over-expression mentioning

confidence: 99%

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A novel role for CRIM1 in the corneal response to UV and pterygium development

Maurizi

Schiroli

Atkinson

et al. 2019

Experimental Eye Research

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Section: Wes Analysis In a Northern Irish Family Affected By Pterygiumentioning

confidence: 99%

Section: Effects Of Wild Type and H412p Mutant Crim1 Over-expression mentioning

confidence: 99%

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A novel role for CRIM1 in the corneal response to UV and pterygium development

Maurizi

Schiroli

Atkinson

et al. 2019

Experimental Eye Research

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“…CRIM1 encodes the cysteine-rich motor neuron 1 protein (CRIM1), which has been characterized as a potential cancer biomarker ( 42 ). It has been reported that increased CRIM1 inhibits the proliferation and migration of vascular endothelial cells ( 43 ). Additionally, increased CRIM1 expression has been reported in drug-resistant myeloid leukemia cells compared with drug-sensitive cells ( 44 ).…”

Section: Discussionmentioning

confidence: 99%

Exploration of the mechanism of colorectal cancer metastasis using microarray analysis

et al. 2017

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The aim of the present study was to investigate the mechanism of metastasis in colorectal cancer (CRC) using microRNA (miRNA) and mRNA expression profiles. The mRNA and miRNA expression profiles of the GSE2509 and GSE56350 datasets were obtained from the Gene Expression Omnibus database. The differentially expressed genes (DEGs) and differentially expressed miRNAs (DEMs) were identified using the limma software package. The Database for Annotation, Visualization and Integrated Discovery was used to perform Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of the DEGs. The predicted target genes associated with the DEMs were identified using the miRWalk database and the enrichment analysis was conducted using the clusterProfiler package. The miRNA-gene molecular interaction network was visualized using the Cytoscape software platform. A total of 544 DEGs and 42 DEMs were identified. DEGs were annotated in 320 GO terms and 11 KEGG pathways. Overall, 366 miRNA-gene pairs were identified and the miRNA-gene network was visualized. Furthermore, the predicted target genes were mainly classified in 12 pathways. The results of the present study suggest that fibronectin type III domain-containing 3B, cysteine rich transmembrane BMP regulator 1 and forkhead box J2 may be potential therapeutic and prognostic targets of metastatic CRC. In addition, pathways in cancer, the Wnt signaling pathway and extracellular matrix-receptor interaction may play a critical role in CRC metastasis.

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Inhibition of angiogenesis and tumor growth by a novel 1,4‐naphthoquinone derivative

Murota

Shinya

Nishiuchi

et al. 2019

Drug Development Research

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Hit, Lead & Candidate Discovery Antiangiogenesis therapy is a promising way for treatment of solid cancers, and many angiogenesis inhibitors that target vascular endothelial growth factor (VEGF) or its receptors have been developed. We explored novel antiangiogenic compounds other than anti‐VEGF drugs by screening our synthetic compound library and found that 6‐thiophen‐3‐yl‐2‐methoxy‐1,4‐naphthoquinone (6‐TMNQ) had potential as a novel angiogenesis inhibitor. This paper describes the effects of 6‐TMNQ on angiogenesis and tumor growth in vitro and in vivo. 6‐TMNQ inhibited serum‐, VEGF‐, and basic fibroblast growth factor (bFGF)‐stimulated proliferation of endothelial cells in a concentration‐dependent manner, but had no effect on the proliferation of fibroblasts. VEGF‐induced activation of VEGF receptor‐2 in endothelial cells was not affected by the compound. 6‐TMNQ markedly abrogated both migration and tube formation of endothelial cells. Orally administered 6‐TMNQ inhibited angiogenesis in response to VEGF or bFGF in mice in a dose‐dependent manner. Furthermore, when tumor‐bearing mice were treated with 6‐TMNQ, increase in tumor size was significantly prevented due to inhibition of angiogenesis in the tumor tissues. These results demonstrate that 6‐TMNQ is an orally available compound that selectively inhibits endothelial cell proliferation and migration, and abrogates angiogenesis, resulting in the prevention of tumor growth. The mechanism of 6‐TMNQ action is different from that of conventional anti‐VEGF drugs.

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Inhibition of the proliferation and acceleration of migration of vascular endothelial cells by increased cysteine-rich motor neuron 1

Cited by 4 publications

References 13 publications

A novel role for CRIM1 in the corneal response to UV and pterygium development

A novel role for CRIM1 in the corneal response to UV and pterygium development

Exploration of the mechanism of colorectal cancer metastasis using microarray analysis

Inhibition of angiogenesis and tumor growth by a novel 1,4‐naphthoquinone derivative

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