circRNA basic information
circBase ID: hsa_circ_0008285
Name: hsa_circ_CDYL
Synonym: circ_0008285
Host Gene: CDYL
Genomic location(hg19): chr6:4891946-4892613:+
Genomic location(hg38): chr6:4891712-4892379:+
Subcellular localization: exosome
 
 
 
 
 
 
 
Disease basic information
MONDO ID:
 0005396
MONDO name: thoracic aortic aneurysm
Disease details: thoracic aortic aneurysm / TAA
Disease DO ID:
 14004
Disease MeSH ID:
 D017545
Disease NCIt ID:
 -
Disease ICD11 ID:
 1383534118
Disease OMIM ID:
 -
Species: Human
Species details: Homo sapiens
Tissue specimen:

aortic tissues
Cell lines:

-
In vivo animal model:

-
circRNA-disease information
Expression pattern:
UP
Associated gene: BASP1
Associated microRNA: miR-150-5p
Biological function: promotes vascular smooth muscle cell apoptosis; inhibits vascular smooth muscle cell proliferation
Molecular mechanism: circ_0008285 acts as a miRNA sponge for miR-150-5p to regulate BASP1 expression (ceRNA mechanism).
Biological pathway or process:

apoptosis (promotes); proliferation (inhibits); ceRNA regulation (other)
Detected method:
Q
Validation methods:

RT-qPCR; RNase R Treatment; Luciferase Reporter Assay; RIP (RNA Immunoprecipitation); Transfection; CCK8; EdU Staining; Annexin V/PI Flow Cytometry; Western Blot; Clinical Sample Validation; Bioinformatics Analysis
Clinical significance:

-
Description:

circ_0008285 is up-regulated in TAA aortic tissue and in Ang II-treated human VSMCs, where it promotes apoptosis and proliferation arrest. Mechanistically, it sponges miR-150-5p to increase BASP1, and it can be packaged into exosomes for intercellular transfer.
Confidence score:

0.7581
Other information
Title:

Circ_0008285 silencing suppresses angiotensin II-induced vascular smooth muscle cell apoptosis in thoracic aortic aneurysm via miR-150-5p/BASP1 axis.

Journal: Thoracic cancer
Published: 2023
PubMed ID: 37337843
Study type:

combined biological and clinical study
Data availability: The data used to support the findings of this study are available from the corresponding author upon request.
Code availability: -