Entry Detail

General Information

Database ID: LDA0004224
Species: Homo sapiens
Confidence Score: 0.985791
Contents: >> ncRNA Information
>> ncRNA Association Statistics
>> Disease Information
>> Disease Association Statistics
>> Evidence Support
>> Reference
Causality: Yes
Clinical Significance: Yes

 


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:AGAP2-AS1
Full Name:AGAP2 antisense RNA 1
Category:LncRNA
Species:Homo sapiens
Synonyms:PUNISHER
Chromosome:12
Strand:+
Coordinate:
Start Site(bp):57726240End Site(bp):57728356
External Links:
Ensembl ID:ENSG00000255737
Ensembl Transcript ID:N/A
Entrez Gene:100130776.0
NONCODE ID:N/A
RefSeq Accession:N/A

 

ncRNA Association Statistics

Total Associated Disease Number:38   
More Information
Causal Disease Number:34
Network:
Top Causal Diseases:
Colorectal Neoplasms  (Score: 0.999893)
Colorectal Neoplasms  (Score: 0.999893)
Glioma  (Score: 0.985791)
Cholangiocarcinoma  (Score: 0.985791)
Prostatic Neoplasms  (Score: 0.985791)
Thyroid Cancer, Papillary  (Score: 0.985791)
Colonic Neoplasms  (Score: 0.985791)
Glioma  (Score: 0.985791)
Colonic Neoplasms  (Score: 0.985791)
Prostatic Neoplasms  (Score: 0.985791)
More Information

 

 

Disease Information

 Disease OntologyMeSH
Disease ID:D005910
Disease Name:Glioma
Category:MeSH
Type:Neoplasms
Define:Benign and malignant central nervous system neoplasms derived from glial cells (i.e., astrocytes, oligodendrocytes, and ependymocytes). Astrocytes may give rise to astrocytomas (ASTROCYTOMA) or glioblastoma multiforme (see GLIOBLASTOMA). Oligodendrocytes give rise to oligodendrogliomas (OLIGODENDROGLIOMA) and ependymocytes may undergo transformation to become EPENDYMOMA; CHOROID PLEXUS NEOPLASMS; or colloid cysts of the third ventricle. (From Escourolle et al., Manual of Basic Neuropathology, 2nd ed, p21)
Alias:Glioma//Gliomas//Glial Cell Tumors//Glial Cell Tumor//Tumor, Glial Cell//Tumors, Glial Cell//Mixed Glioma//Glioma, Mixed//Gliomas, Mixed//Mixed Gliomas//Malignant Glioma//Glioma, Malignant//Gliomas, Malignant//Malignant Gliomas

 

Disease Association Statistics

Total Associated ncRNA Number:660   
More Information
Causal ncRNA Number:606
Network:
Top Causal ncRNAs:
H19  (Score: 1)
H19  (Score: 1)
MEG3  (Score: 1)
UCA1  (Score: 1)
UCA1  (Score: 1)
GAS5  (Score: 1)
FOXD2-AS1  (Score: 1)
NEAT1  (Score: 1)
MEG3  (Score: 1)
PVT1  (Score: 1)
More Information

 

Evidence Support

Strong Evidence:CCK8//qRT-PCR
Weak Evidence:

 

Reference

[1] PubMed ID:30684575
Disease Name:Glioma
Sample:glioma tissue and cell lines
Dysfunction Pattern:Regulation[Wnt/β-catenin signaling pathway]
Validated Method:qRT-PCR
Description:In this study, we found that lncRNA AGAP2-AS1 was differentially expressed in glioma tissue samples and cell lines.Higher expression of AGAP2-AS1 was correlated with the lower overall survival of glioma patients. Mechanistically, AGAP2-AS1 upregulated HDGF by sponging miR-15a/b-5p. The function of AGAP2-AS1-miR-15a/b-5p-HDGF axis was confirmed by performing rescue assays. Experimental results suggested that miR-15a/b-5p and HDGF involved in AGAP2-AS1-mediated glioma cell proliferation. Moreover, AGAP2-AS1 and HDGF were found to activate Wnt/β-catenin signaling pathway in glioma cell lines. In summary, this study demonstrated that AGAP2-AS1 promoted glioma cell proliferation by sponging miR-15a/b-5p to upregulate the expression of HDGF.
Causality:Yes
Causal Description:Functionally, AGAP2-AS1 knockdown inhibited glioma cell proliferation and accelerated glioma cell apoptosis.
Clinical-realted Application:Higher expression of AGAP2-AS1 was correlated with the lower overall survival of glioma patients.

[2] PubMed ID:30525219
Disease Name:Glioma
Sample:glioma tissues
Dysfunction Pattern:Expression[Expression[Expression[highly expressed]-expression]-expression]
Validated Method:CCK8//qRT-PCR
Description:In our results, we found AGAP2-AS1 expression was increased in GBM compared with adjacent normal brain tissues or low-grade glioma tissues, and there was no significantly different between low-grade glioma tissues and normal tissues.
Causality:Yes
Causal Description:The loss-of-function studies showed that Expression[down-expression]regulation of AGAP2-AS1 depressed cell proliferation, migration, and invasion, and promoted cell apoptosis in GBM.
Clinical-realted Application:Kaplan-Meier survival analysis indicated patients with GBM having high-expression of AGAP2-AS1 had shorter overall survival time than those with low expression of AGAP2-AS1.