Entry Detail


General Information

Database ID: LDA0006521
Species: Homo sapiens
Confidence Score: 0.731059
Contents: >> ncRNA Information
>> ncRNA Association Statistics
>> Disease Information
>> Disease Association Statistics
>> Evidence Support
>> Reference
Causality: Yes
Clinical Significance: Unknown

 


ncRNA Information

Reference Genome Note: GRCh38 for human lncRNAs; GRCm39 for mouse lncRNAs; mRatBN7.2 for rat lncRNAs; hg19 for human circRNAs; mm9 for mouse circRNAs.

ncRNA Symbol:SPRR2C
Full Name:small proline rich protein 2C (pseudogene)
Category:LncRNA
Species:Homo sapiens
Synonyms:-
Chromosome:1
Strand:-
Coordinate:
Start Site(bp):153140116End Site(bp):153141532
External Links:
Ensembl ID:ENSG00000229035
Ensembl Transcript ID:N/A
Entrez Gene:6702.0
NONCODE ID:N/A
RefSeq Accession:N/A

 

ncRNA Association Statistics

Total Associated Disease Number:4   
More Information
Causal Disease Number:2
Network:
Top Causal Diseases:
Psoriasis  (Score: 0.731059)
Psoriasis  (Score: 0.731059)
More Information

 

 

Disease Information

 Disease OntologyMeSH
Disease ID:DOID:8893D011565
Disease Name:psoriasisPsoriasis
Category:Disease OntologyMeSH
Type:Skin and Connective Tissue Diseases
Define:A skin disease that is characterized by patches of thick red skin and silvery scales.A common genetically determined, chronic, inflammatory skin disease characterized by rounded erythematous, dry, scaling patches. The lesions have a predilection for nails, scalp, genitalia, extensor surfaces, and the lumbosacral region. Accelerated epidermopoiesis is considered to be the fundamental pathologic feature in psoriasis.
Alias:Psoriasis//Psoriases//Pustulosis of Palms and Soles//Pustulosis Palmaris et Plantaris//Palmoplantaris Pustulosis//Pustular Psoriasis of Palms and Soles

 

Disease Association Statistics

Total Associated ncRNA Number:28   
More Information
Causal ncRNA Number:18
Network:
Top Causal ncRNAs:
HOTAIR  (Score: 0.731059)
NORAD  (Score: 0.731059)
Meg3  (Score: 0.731059)
SPRR2C  (Score: 0.731059)
circVAPA  (Score: 0.731059)
circEIF5  (Score: 0.731059)
XIST  (Score: 0.731059)
AGAP2-AS1  (Score: 0.731059)
chr2:206992521|206994966  (Score: 0.731059)
HOTAIR  (Score: 0.731059)
More Information

 

Evidence Support

Strong Evidence:Transfection//Immunoblotting//qRT-PCR//MTT//H&E Staining//IHC//EdU Staining
Weak Evidence:

 

Reference

[1] PubMed ID:33452236
Disease Name:Psoriasis
Sample:psoriatic lesion samples and HaCaT cell lines
Dysfunction Pattern:Regulation(miR-330/STAT1/S100A7 axis)
Validated Method:Transfection//Immunoblotting//qRT-PCR//MTT//H&E Staining//IHC//EdU Staining
Description: SPRR2C expression was significantly upregulated in both psoriatic lesion samples and HaCaT cell lines in response to IL-22 treatment. After SPRR2C knockdown, IL-22-induced suppression of HaCaT proliferation, changes in the KRT5/14/1/10 protein levels, and suppression of the IL-1β, IL-6, and TNF-α mRNA levels were dramatically reversed. In the coexpression network with SPRR2C based on GSE114286, miR-330 was significantly negatively correlated with SPRR2C, while STAT1 and S100A7 were positively correlated with SPRR2C. By binding to miR-330, SPRR2C competed with STAT1 and S100A7 to counteract miR-330-mediated suppression of STAT1 and S100A7. MiR-330 overexpression also reversed the IL-22-induced changes in HaCaT cell lines; in response to IL-22 treatment, miR-330 inhibition significantly attenuated the effects of SPRR2C knockdown. STAT1 and S100A7 expression was significantly upregulated in psoriatic lesion samples. The expression of miR-330 had a negative correlation with the expression of SPRR2C, while the expression of SPRR2C had a positive correlation with the expression of STAT1 and S100A7. Thus, SPRR2C modulates the IL-22-stimulated HaCaT cell phenotype through the miR-330/STAT1/S100A7 axis. WGCNA might uncover additional biological pathways that are crucial in the pathogenesis and response to the treatment of psoriasis.
Causality:Yes
Causal Description:After SPRR2C knockdown, IL-22-induced suppression of HaCaT proliferation, changes in the KRT5/14/1/10 protein levels, and suppression of the IL-1β, IL-6, and TNF-α mRNA levels were dramatically reversed.
Clinical-realted Application: