circRNA basic information
circBase ID: -
Name: hsa_circ_ITCH
Synonym: circITCH
Host Gene: ITCH
Genomic location(hg19): -
Genomic location(hg38): -
Subcellular localization: not tested
 
 
 
 
 
 
 
Disease basic information
MONDO ID:
0011385
MONDO name: intervertebral disk degenerative disorder
Disease details: intervertebral disc degeneration
Disease DO ID:
90
Disease MeSH ID:
D055959
Disease NCIt ID:
C26983
Disease ICD11 ID:
-
Disease OMIM ID:
603932
Species: Human
Species details: Homo sapiens
Tissue specimen:

nucleus pulposus (NP) tissues

Cell lines:

-

In vivo animal model:

-

circRNA-disease information
Expression pattern:
UP
Associated gene: SOX4, Wnt/beta-catenin pathway
Associated microRNA: miR-17-5p
Biological function: Promotes apoptosis, inhibits proliferation, and promotes extracellular matrix (ECM) degradation in nucleus pulposus (NP) cells during IDD progression.
Molecular mechanism: Acts as a miR-17-5p sponge to de-repress SOX4 and activate Wnt/beta-catenin signaling, thereby promoting ECM degradation.
Biological pathway or process:

Wnt/beta-catenin (promotes); apoptosis (promotes); proliferation (inhibits); other pathway/process (promotes); ceRNA regulation (promotes)

Detected method:
Q
Validation methods:

RT-qPCR; Clinical Sample Validation; Bioinformatics Analysis; Luciferase Reporter Assay; Transfection; CCK8; Annexin V/PI Flow Cytometry; Western Blot

Clinical significance:

-

Description:

circITCH is up-regulated in IDD nucleus pulposus tissues and promotes NP-cell apoptosis, suppresses proliferation, and accelerates ECM degradation. Mechanistically, circITCH sponges miR-17-5p to increase SOX4 and activate Wnt/beta-catenin signaling, driving degenerative changes.

Confidence score:

0.6479

Other information
Title:

Circular RNA ITCH promotes extracellular matrix degradation via activating Wnt/beta-catenin signaling in intervertebral disc degeneration.

Journal: Aging
Published: 2021
PubMed ID: 34015763
Study type:

combined biological and clinical study

Data availability: -
Code availability: -