circRNA basic information
circBase ID: -
Name: hsa_circ_IGF1R
Synonym: circ-insulin-like growth factor 1 receptor
Host Gene: -
Genomic location(hg19): -
Genomic location(hg38): -
Subcellular localization: not tested
 
 
 
 
 
 
 
Disease basic information
MONDO ID:
0005083
MONDO name: psoriasis
Disease details: psoriasis
Disease DO ID:
8893
Disease MeSH ID:
D011565
Disease NCIt ID:
C3346
Disease ICD11 ID:
63698555
Disease OMIM ID:
-
Species: Human
Species details: Homo sapiens
Tissue specimen:

-

Cell lines:

HaCaT; 293T

In vivo animal model:

-

circRNA-disease information
Expression pattern:
UP
Associated gene: CDK1
Associated microRNA: miR-194-5p
Biological function: circ-IGF1R promotes proliferation, migration and invasion, and inhibits apoptosis in IL-22-stimulated HaCaT cells.
Molecular mechanism: circ-IGF1R regulates the miR-194-5p/CDK1 axis; miR-194-5p is a target of circ-IGF1R and CDK1 is targeted by miR-194-5p.
Biological pathway or process:

proliferation (promotes); migration (promotes); invasion (promotes); apoptosis (inhibits); ceRNA regulation (other)

Detected method:
Q
Validation methods:

RT-qPCR; Bioinformatics Analysis; Luciferase Reporter Assay; Transfection; MTT; Transwell Assay; Annexin V/PI Flow Cytometry; Western Blot

Clinical significance:

circ-IGF1R may serve as a potential treatment target for psoriasis.

Description:

In an IL-22-stimulated HaCaT cell model of psoriasis, circ-IGF1R is up-regulated and promotes keratinocyte proliferation, migration and invasion while inhibiting apoptosis. Mechanistically, circ-IGF1R acts through the miR-194-5p/CDK1 axis, and knockdown of circ-IGF1R reverses psoriasis-like cellular phenotypes, suggesting a potential therapeutic target.

Confidence score:

0.5607

Other information
Title:

Circ-IGF1R plays a significant role in psoriasis via regulation of a miR-194-5p/CDK1 axis.

Journal: Cytotechnology
Published: 2021
PubMed ID: 34776628
Study type:

biological research

Data availability: The datasets used and/or analyzed during the current study are available from the corresponding author upon reasonable request.
Code availability: -