circRNA basic information
circBase ID: hsa_circ_0113656
Name: hsa_circ_DHCR24
Synonym: circ_0113656 / circDHCR24
Host Gene: DHCR24
Genomic location(hg19): -
Genomic location(hg38): -
Subcellular localization: not tested
 
 
 
 
 
 
 
Disease basic information
MONDO ID:
0005311
MONDO name: atherosclerosis
Disease details: atherosclerosis / AS
Disease DO ID:
1936
Disease MeSH ID:
D050197
Disease NCIt ID:
C35768
Disease ICD11 ID:
109367356
Disease OMIM ID:
-
Species: Human
Species details: Homo sapiens
Tissue specimen:

blood

Cell lines:

HVSMCs

In vivo animal model:

-

circRNA-disease information
Expression pattern:
UP
Associated gene: IGF2
Associated microRNA: miR-188-3p
Biological function: Promotes ox-LDL-induced HVSMC proliferation, migration, invasion and related injury; its knockdown attenuates these effects.
Molecular mechanism: Acts as a miR-188-3p sponge to regulate IGF2 expression in ox-LDL-treated HVSMCs.
Biological pathway or process:

proliferation (promotes); migration (promotes); invasion (promotes); ceRNA regulation (promotes)

Detected method:
Q
Validation methods:

RT-qPCR; RNase R Treatment; Clinical Sample Validation; Transfection; CCK8; EdU Staining; Transwell Assay; Wound Healing Assay; Western Blot; RIP (RNA Immunoprecipitation); Luciferase Reporter Assay

Clinical significance:

-

Description:

circ_0113656 (circDHCR24) is up-regulated in blood from atherosclerosis patients and in ox-LDL-treated HVSMCs. It promotes ox-LDL-induced HVSMC proliferation, migration and invasion by sponging miR-188-3p, thereby increasing IGF2; circ_0113656 knockdown alleviates these injury phenotypes via the miR-188-3p/IGF2 axis.

Confidence score:

0.7412

Other information
Title:

Knockdown of circ_0113656 assuages oxidized low-density lipoprotein-induced vascular smooth muscle cell injury through the miR-188-3p/IGF2 pathway.

Journal: Open medicine (Warsaw, Poland)
Published: 2023
PubMed ID: 37415611
Study type:

combined biological and clinical study

Data availability: The analyzed data sets generated during the present study are available from the corresponding author on reasonable request.
Code availability: -