HCSGD entry for MIR22


1. General information

Official gene symbolMIR22
Entrez ID407004
Gene full namemicroRNA 22
Other gene symbolsMIRN22 hsa-mir-22 miR-22
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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This gene isn't in Literature mining network.

3. Gene ontology annotation

Not in the Gene ontology

4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.99694216790.02780309260.99999024730.3172107499

  • Individual experiment result
    ( "-" represent NA in the specific microarray platform )

Data sourceUp or downLog fold change
GSE11954--
GSE13712_SHEAR--
GSE13712_STATIC--
GSE19018--
GSE19899_A1--
GSE19899_A2--
PubMed_21979375_A1--
PubMed_21979375_A2--
GSE35957--
GSE36640--
GSE54402--
GSE9593--
GSE43922--
GSE24585--
GSE37065--
GSE28863_A1Down-0.0538982546
GSE28863_A2Down-0.6925241255
GSE28863_A3Down-0.9577625454
GSE28863_A4Up0.1387395151
GSE48662--

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Not regulated by compounds

  • Drugs

Not regulated by drugs

  • MicroRNAs

  • mirTarBase
No target information from mirTarBase
  • mirRecord
No target information from mirRecord

6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 3 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

25323119Here, we investigated the significance and molecular mechanisms of microRNA-22 (miR-22) governing EPC senescence
25323119RESULTS: We found that miR-22 was upregulated in aged EPCs
25323119Overexpression of miR-22 in young EPCs induced cell senescence, decreased proliferation and migration, and impaired angiogenesis in vitro
25323119Conversely, silencing of endogenous miR-22 led to decreased cell senescence, increased proliferation and migration, and improved angiogenesis
25323119AKT3 was identified as a direct target of miR-22, and restoration of AKT3 expression attenuated the effects of miR-22 in young EPCs
25323119CONCLUSION: Our results indicate that miR-22 induces EPC senescence by downregulating AKT3 expression, providing a potential novel target for the reversal of EPC dysfunction in angiogenesis
22538858MiR-22 was most prominently upregulated during cardiac aging
22538858Luciferase reporter assays validated mimecan as a bona fide miR-22 target
22538858Both, miR-22 and its target mimecan were co- expressed in cardiac fibroblasts and smooth muscle cells
22538858Functionally, miR-22 overexpression induced cellular senescence and promoted migratory activity of cardiac fibroblasts
22538858Rescue experiments revealed that the effects of miR-22 on cardiac fibroblasts were only partially mediated by mimecan
22538858In conclusion, miR-22 upregulation in the aging heart contributed at least partly to accelerated cardiac fibroblast senescence and increased migratory activity
22538858Our results suggest an involvement of miR-22 in age-associated cardiac changes, such as cardiac fibrosis
21502362Here, we report that miR-22, a novel SA-miRNA, has an impact on tumorigenesis
21502362Synthetic miR-22 delivery suppresses tumor growth and metastasis in vivo by inducing cellular senescence in a mouse model of breast carcinoma
21502362Our study provides the first evidence that miR-22 restores the cellular senescence program in cancer cells and acts as a tumor suppressor
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