Accession ID: MIRT004597 [miRNA, hsa-miR-31 :: CASR, target gene]
|Synonyms||MIRN31, hsa-mir-31, miR-31, MIR31|
|Description||Homo sapiens miR-31 stem-loop|
|Comment||The mature sequence shown here represents the most commonly cloned form from large-scale cloning studies . The 5' end of the miRNA may be offset with respect to previous annotations.|
|2nd Structure of pre-miRNA|
|Mature Sequence||44| UGCUAUGCCAACAUAUUGCCAU |65|
|Putative hsa-miR-31-3p Targets|
|Mature Sequence||8| AGGCAAGAUGCUGGCAUAGCU |28|
|Putative hsa-miR-31-5p Targets|
|Synonyms||CAR, EIG8, FHH, FIH, GPRC2A, HHC, HHC1, MGC138441, NSHPT, PCAR1|
|Putative miRNA Targets on CASR|
|3'UTR of CASR
(miRNA target sites are highlighted)
>CASR|NM_000388|3'UTR 1 TAAAATGGAAGGAGAAGACTGGGCTAGGGAGAATGCAGAGAGGTTTCTTGGGGTCCCAGGGAAGAGGAATCGCCCCAGAC 81 TCCTTTCCTCTGAGGAAGAAGGGATAATAGACACATCAAATGCCCCGAATTTAGTCACACCATCTTAAATGACAGTGAAT 161 TGACCCATGTTCCCTTTAAAATTAAAAAAAAGAAGAGCCTTGTGTTTCTGTGGTTGCATTTGTCAAAGCATTGAGATCTC 241 CACGGTCAGATTTGCTGTTCACCCACATCTAATGTCTCTTCCTCTGTTCTATCCCACCCAACAGCTCAGAGATGAAACTA 321 TGGCTTTAAACTACCCTCCAGAGTGTGCAGACTGATGGGACATCAAATTTGCCACCACTAGAGCTGAGAGTCTGAAAGAC 401 AGAATGTCACCAGTCCTGCCCAATGCCTTGACAACAGACTGAATTTTAAATGTTCACAACATAAGGAGAATGTATCTCCT 481 CCTATTTATGAAAACCATATGATATTTTGTCTCCTACCTGCTGCTGCTATTATGTAACATCCAGAAGGTTTGCACCCCTC 561 CTATACCATATGTCTGCTTCTGTCCAGGACATGATACTGATGCCATGTTTAGATTCCAGGATCACAAGAATCACCTCAAA 641 TTGTTAGGAAGGGACTGCATAAACCAATGAGCTGTATCTGTAATTAATATTCCTATATGTAGCTTTATCCTTAGGAAAAT 721 GCTTCTGTTGTAATAGTCCATGGACAATATAAACTGAAAAATGTCAGTCTGGTTTATATAAGGCAGTATTATTGAGCTCT 801 ATTTCCCCACCCCACTATCCTCACTCCCATAAGCTAAGCCTTATGTGAGCCCCTTCAGGGACTCAAGGGTCCAGAAGTCC 881 CTCCCATCTCTACCCCAAAGAATTCCTGAAGCCAGATCCACCCTATCCCTGTACAGAGTAAGTTCTCAATTATTGGCCTG 961 CTAATAGCTGCTAGGGTAGGAAAGCGTGGTTCCAAGAAAGATCCACCCTCAAATGTCAGAGCTATGTTCCCTCCAGCAGT 1041 GGTATTAATACTGCCGGTCACCCAGGCTCTGGAGCCAGAGAGACAGACCGGGGTTCAAGCCATGGCTTCGTCATTTGCAA 1121 GCTGAGTGACTGTAGGCAGGGAACCTTAACCTCTCTAAGCCACAGCTTCTTCATCTTTAAAATAAGGATAATAATCATTC 1201 TTTCCCCTCAGAGCTCTTATGTGGATTAAACGAGATAATGTATATAAAGTACTTTAGCCTGGTACCTAGCACACAATAAG 1281 CATTCAATAAATATTAGTTAATATTATTAAAAAAAAAA
|miRNA-target interactions (Predicted by miRanda)||
|miRNA:Target||hsa-miR-31 :: CASR [ Functional MTI ]|
|Validation Method||LacZ assay|
|Location of target site||3'UTR|
|Tools used in this research||PicTar, TargetScan|
|Original Description (Extracted from the article)||... miR-31 expression repressed FIH expression and mutations within the predictive miR-31 target site in the FIH 3' UTR abrogated FIH repression ...
- Liu, C. J. Tsai, M. M. Hung, P. S. Kao, S. et al., 2010, Cancer Res.
miR-31 ablates expression of the HIF regulatory factor FIH to activate the HIF pathway in head and neck carcinoma- Liu, C. J. Tsai, M. M. Hung, P. S. Kao, S. et al.
- Cancer Res, 2010
MicroRNAs (miRNA) are endogenously expressed noncoding RNAs with important biological and pathological functions that are yet to be fully defined. This study investigated alterations in miRNA expression in head and neck squamous cell carcinoma (HNSCC), the incidence of which is rising throughout the world. Initial screening and subsequent analysis identified a panel of aberrantly expressed miRNAs in HNSCC tissues, with miR-31 among the most markedly upregulated. Ectopic expression of miR-31 increased the oncogenic potential of HNSCC cells under normoxic conditions in cell culture or tumor xenografts. Conversely, blocking miR-31 expression reduced the growth of tumor xenografts. The in silico analysis suggested that miR-31 may target the 3' untranslated region (UTR) of factor-inhibiting hypoxia-inducible factor (FIH), a hypoxia-inducible factor (HIF) regulatory factor that inhibits the ability of HIF to act as a transcriptional regulator under normoxic conditions. In support of this likelihood, miR-31 expression repressed FIH expression and mutations within the predictive miR-31 target site in the FIH 3' UTR abrogated FIH repression. Furthermore, miR-31 expression increased HIF transactivation activity. We found that FIH suppressed oncogenic phenotypes under normoxic conditions and that this activity was abrogated by functional mutations. Lastly, increased miR-31 expression was correlated with decreased levels of FIH in tumor tissues. Our findings suggest that miR-31 contributes to the development of HNSCC by impeding FIH to activate HIF under normoxic conditions.LinkOut: [PMID: 20145132]