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http://purl.uniprot.org/citations/32390601http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/32390601http://www.w3.org/2000/01/rdf-schema#comment"

Background

Immunosuppressive receptor LILRB1 regulates tumors progression by transducing immune inhibitory signals via intracellular immunoreceptor tyrosine-based inhibitory motifs. However, its role in Hepatocellular Carcinoma (HCC) remains vague.

Objective

This study is aimed to disclose the association between LILRB1 and HCC.

Methods

Immunoblotting and qRT-PCR were employed to evaluate the level of LILRB1 in hepatocarcinoma cells. LILRB1-positive cells in tissue array were measured using immunohistochemistry staining. The relation among LILRB1, SHP1 and SHP2 and survival rates were analyzed using Gene Expression Profiling Interactive Analysis (GEPIA) and Oncomine database.

Results

LILRB1 was robustly reduced in hepatocarcinoma cells compared to normal cells. Clinically, LILRB1 was significantly higher in 49 of 75 (65%) paired paracarcinoma tissues than that in paired HCC samples. 48 of 75 (64%) HCC subjects in tissue microarray showed low level of LILRB1, compared to 25 of 75 (33%) in paired-adjacent tissues. Oncomine database and GEPIA analysis confirmed that LILRB1 was lower in HCC than normal tissues. Additionally, lowLILRB1 had a significant association with clinicopathological characteristics and Disease Free Survival, but no association with Overall Survival in HCC patients. Mechanismly, positive correlation between LILRB1 and SHP1, but not SHP2 was observed in HCC.

Conclusions

LILRB1 possibly plays an antitumor effect in hepatocarcinoma cells by integrating SHP1, providing evidence that LILRB1 might be involved in the pathologic progression of HCC."xsd:string
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http://purl.uniprot.org/citations/32390601http://purl.uniprot.org/core/author"Chen S."xsd:string
http://purl.uniprot.org/citations/32390601http://purl.uniprot.org/core/author"Chen P."xsd:string
http://purl.uniprot.org/citations/32390601http://purl.uniprot.org/core/author"Cheng J."xsd:string
http://purl.uniprot.org/citations/32390601http://purl.uniprot.org/core/author"Cheng F."xsd:string
http://purl.uniprot.org/citations/32390601http://purl.uniprot.org/core/author"Jiang P."xsd:string
http://purl.uniprot.org/citations/32390601http://purl.uniprot.org/core/author"Zhang R."xsd:string
http://purl.uniprot.org/citations/32390601http://purl.uniprot.org/core/author"Gou X."xsd:string
http://purl.uniprot.org/citations/32390601http://purl.uniprot.org/core/author"Luan J."xsd:string
http://purl.uniprot.org/citations/32390601http://purl.uniprot.org/core/author"Kuang X."xsd:string
http://purl.uniprot.org/citations/32390601http://purl.uniprot.org/core/date"2020"xsd:gYear
http://purl.uniprot.org/citations/32390601http://purl.uniprot.org/core/name"Cancer Biomark"xsd:string
http://purl.uniprot.org/citations/32390601http://purl.uniprot.org/core/pages"309-319"xsd:string
http://purl.uniprot.org/citations/32390601http://purl.uniprot.org/core/title"Immunosuppressive receptor LILRB1 acts as a potential regulator in hepatocellular carcinoma by integrating with SHP1."xsd:string
http://purl.uniprot.org/citations/32390601http://purl.uniprot.org/core/volume"28"xsd:string
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