| pre-miRNA Information | |
|---|---|
| pre-miRNA | hsa-mir-26a-1 |
| Genomic Coordinates | chr3: 37969404 - 37969480 |
| Synonyms | MIR26A, MIRN26A1, MIR26A1 |
| Description | Homo sapiens miR-26a-1 stem-loop |
| Comment | The mature sequence shown here represents the most commonly cloned form from large-scale cloning studies . |
| RNA Secondary Structure |  |
| Associated Diseases |  |
| pre-miRNA | hsa-mir-26a-2 |
| Genomic Coordinates | chr12: 57824609 - 57824692 |
| Synonyms | MIRN26A2, MIR26A2 |
| Description | Homo sapiens miR-26a-2 stem-loop |
| Comment | miR-26a was cloned from HeLa cells . |
| RNA Secondary Structure | |
| Associated Diseases |  |
| Mature miRNA Information | ||||||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Mature miRNA | hsa-miR-26a-5p | |||||||||||||||||||||||||||
| Sequence | 10| UUCAAGUAAUCCAGGAUAGGCU |31 | |||||||||||||||||||||||||||
| Evidence | Experimental | |||||||||||||||||||||||||||
| Experiments | Cloned | |||||||||||||||||||||||||||
| Editing Events in miRNAs |
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DRVs in miRNA |
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| SNPs in miRNA |
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| Putative Targets | ||||||||||||||||||||||||||||
| miRNA Expression profile | |
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| Human miRNA Tissue Atlas | |
| miRNAs in Extracellular Vesicles |
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| Circulating MicroRNA Expression Profiling | |
| Biomarker Information |
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| Gene Information | |||||||||||||||||||||
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| Gene Symbol | PTEN | ||||||||||||||||||||
| Synonyms | 10q23del, BZS, CWS1, DEC, GLM2, MHAM, MMAC1, PTEN1, PTENbeta, TEP1 | ||||||||||||||||||||
| Description | phosphatase and tensin homolog | ||||||||||||||||||||
| Transcript | NM_000314 | ||||||||||||||||||||
| Expression | |||||||||||||||||||||
| Putative miRNA Targets on PTEN | |||||||||||||||||||||
| 3'UTR of PTEN (miRNA target sites are highlighted) |
>PTEN|NM_000314|3'UTR 1 ATTTTTTTTTATCAAGAGGGATAAAACACCATGAAAATAAACTTGAATAAACTGAAAATGGACCTTTTTTTTTTTAATGG 81 CAATAGGACATTGTGTCAGATTACCAGTTATAGGAACAATTCTCTTTTCCTGACCAATCTTGTTTTACCCTATACATCCA 161 CAGGGTTTTGACACTTGTTGTCCAGTTGAAAAAAGGTTGTGTAGCTGTGTCATGTATATACCTTTTTGTGTCAAAAGGAC 241 ATTTAAAATTCAATTAGGATTAATAAAGATGGCACTTTCCCGTTTTATTCCAGTTTTATAAAAAGTGGAGACAGACTGAT 321 GTGTATACGTAGGAATTTTTTCCTTTTGTGTTCTGTCACCAACTGAAGTGGCTAAAGAGCTTTGTGATATACTGGTTCAC 401 ATCCTACCCCTTTGCACTTGTGGCAACAGATAAGTTTGCAGTTGGCTAAGAGAGGTTTCCGAAGGGTTTTGCTACATTCT 481 AATGCATGTATTCGGGTTAGGGGAATGGAGGGAATGCTCAGAAAGGAAATAATTTTATGCTGGACTCTGGACCATATACC 561 ATCTCCAGCTATTTACACACACCTTTCTTTAGCATGCTACAGTTATTAATCTGGACATTCGAGGAATTGGCCGCTGTCAC 641 TGCTTGTTGTTTGCGCATTTTTTTTTAAAGCATATTGGTGCTAGAAAAGGCAGCTAAAGGAAGTGAATCTGTATTGGGGT 721 ACAGGAATGAACCTTCTGCAACATCTTAAGATCCACAAATGAAGGGATATAAAAATAATGTCATAGGTAAGAAACACAGC 801 AACAATGACTTAACCATATAAATGTGGAGGCTATCAACAAAGAATGGGCTTGAAACATTATAAAAATTGACAATGATTTA 881 TTAAATATGTTTTCTCAATTGTAACGACTTCTCCATCTCCTGTGTAATCAAGGCCAGTGCTAAAATTCAGATGCTGTTAG 961 TACCTACATCAGTCAACAACTTACACTTATTTTACTAGTTTTCAATCATAATACCTGCTGTGGATGCTTCATGTGCTGCC 1041 TGCAAGCTTCTTTTTTCTCATTAAATATAAAATATTTTGTAATGCTGCACAGAAATTTTCAATTTGAGATTCTACAGTAA 1121 GCGTTTTTTTTCTTTGAAGATTTATGATGCACTTATTCAATAGCTGTCAGCCGTTCCACCCTTTTGACCTTACACATTCT 1201 ATTACAATGAATTTTGCAGTTTTGCACATTTTTTAAATGTCATTAACTGTTAGGGAATTTTACTTGAATACTGAATACAT 1281 ATAATGTTTATATTAAAAAGGACATTTGTGTTAAAAAGGAAATTAGAGTTGCAGTAAACTTTCAATGCTGCACACAAAAA 1361 AAAGACATTTGATTTTTCAGTAGAAATTGTCCTACATGTGCTTTATTGATTTGCTATTGAAAGAATAGGGTTTTTTTTTT 1441 TTTTTTTTTTTTTTTTTTTAAATGTGCAGTGTTGAATCATTTCTTCATAGTGCTCCCCCGAGTTGGGACTAGGGCTTCAA 1521 TTTCACTTCTTAAAAAAAATCATCATATATTTGATATGCCCAGACTGCATACGATTTTAAGCGGAGTACAACTACTATTG 1601 TAAAGCTAATGTGAAGATATTATTAAAAAGGTTTTTTTTTCCAGAAATTTGGTGTCTTCAAATTATACCTTCACCTTGAC 1681 ATTTGAATATCCAGCCATTTTGTTTCTTAATGGTATAAAATTCCATTTTCAATAACTTATTGGTGCTGAAATTGTTCACT 1761 AGCTGTGGTCTGACCTAGTTAATTTACAAATACAGATTGAATAGGACCTACTAGAGCAGCATTTATAGAGTTTGATGGCA 1841 AATAGATTAGGCAGAACTTCATCTAAAATATTCTTAGTAAATAATGTTGACACGTTTTCCATACCTTGTCAGTTTCATTC 1921 AACAATTTTTAAATTTTTAACAAAGCTCTTAGGATTTACACATTTATATTTAAACATTGATATATAGAGTATTGATTGAT 2001 TGCTCATAAGTTAAATTGGTAAAGTTAGAGACAACTATTCTAACACCTCACCATTGAAATTTATATGCCACCTTGTCTTT 2081 CATAAAAGCTGAAAATTGTTACCTAAAATGAAAATCAACTTCATGTTTTGAAGATAGTTATAAATATTGTTCTTTGTTAC 2161 AATTTCGGGCACCGCATATTAAAACGTAACTTTATTGTTCCAATATGTAACATGGAGGGCCAGGTCATAAATAATGACAT 2241 TATAATGGGCTTTTGCACTGTTATTATTTTTCCTTTGGAATGTGAAGGTCTGAATGAGGGTTTTGATTTTGAATGTTTCA 2321 ATGTTTTTGAGAAGCCTTGCTTACATTTTATGGTGTAGTCATTGGAAATGGAAAAATGGCATTATATATATTATATATAT 2401 AAATATATATTATACATACTCTCCTTACTTTATTTCAGTTACCATCCCCATAGAATTTGACAAGAATTGCTATGACTGAA 2481 AGGTTTTCGAGTCCTAATTAAAACTTTATTTATGGCAGTATTCATAATTAGCCTGAAATGCATTCTGTAGGTAATCTCTG 2561 AGTTTCTGGAATATTTTCTTAGACTTTTTGGATGTGCAGCAGCTTACATGTCTGAAGTTACTTGAAGGCATCACTTTTAA 2641 GAAAGCTTACAGTTGGGCCCTGTACCATCCCAAGTCCTTTGTAGCTCCTCTTGAACATGTTTGCCATACTTTTAAAAGGG 2721 TAGTTGAATAAATAGCATCACCATTCTTTGCTGTGGCACAGGTTATAAACTTAAGTGGAGTTTACCGGCAGCATCAAATG 2801 TTTCAGCTTTAAAAAATAAAAGTAGGGTACAAGTTTAATGTTTAGTTCTAGAAATTTTGTGCAATATGTTCATAACGATG 2881 GCTGTGGTTGCCACAAAGTGCCTCGTTTACCTTTAAATACTGTTAATGTGTCATGCATGCAGATGGAAGGGGTGGAACTG 2961 TGCACTAAAGTGGGGGCTTTAACTGTAGTATTTGGCAGAGTTGCCTTCTACCTGCCAGTTCAAAAGTTCAACCTGTTTTC 3041 ATATAGAATATATATACTAAAAAATTTCAGTCTGTTAAACAGCCTTACTCTGATTCAGCCTCTTCAGATACTCTTGTGCT 3121 GTGCAGCAGTGGCTCTGTGTGTAAATGCTATGCACTGAGGATACACAAAAATACCAATATGATGTGTACAGGATAATGCC 3201 TCATCCCAATCAGATGTCCATTTGTTATTGTGTTTGTTAACAACCCTTTATCTCTTAGTGTTATAAACTCCACTTAAAAC 3281 TGATTAAAGTCTCATTCTTGTCATTGTGTGGGTGTTTTATTAAATGAGAGTTTATAATTCAAATTGCTTAAGTCCATTGA 3361 AGTTTTAATTAATGGGCAGCCAAATGTGAATACAAAGTTTTCAGTTTTTTTTTTTCCTGCTGTCCTTCAAAGCCTACTGT 3441 TTAAAAAAAAAAAAAAAAAAAAACATGGCCTGAGAGTAGAGTATCTGTCTACTCATGTTTAATTAAGGAAAAACACTTAT 3521 TTTTAGGGCTTTAGTCATCACTTCATAAATTGTATAAGCACATTAAATAGCGTTCTAGTCCTGAAAAAGTCCAAGATTCT 3601 TAGAAAATTGTGCATATTTTTATTATGACAGATGTTTGAAGATAATTCCCCAGAATGGATTTGATACTTTAGATTTCAAT 3681 TTTGTGGCTTTTGTCTATTATTCTGTACTCTGCCATCAGCATATGGAAAGCTTCATTTACTCATCATGACTTGTGCCATA 3761 TAAAAATTGATATTTCGGAATAGTCTAAAGGACTTTTTGTACTTGAATTTAATCATGTTGTTTCTAATATTCTTAAAAGC 3841 TTGAAGACTAAAGCATATCCTTTCAACAAAGCATAGTAAGGTAATAAGAAAGTGTAGTTTGTACAAGTGTTAAAAAAATA 3921 AAGTAGACAATGTTACAGTGGGACTTATTATTTCAAGTTTACATTTTCTCCATGTAATTTTTTAAAAAGTAAATGAAAAA 4001 ATGTGCAATAATGTAAAATATGAAGTGTATGTGTACACACATTTTATTTTTCGGTATCTTGGGTATACGTATGGTTGAAA 4081 ACTATACTGGAGTCTAAAAGTATTCTAATTTATAAGAAGACATTTTGGTGATGTTTGAAAAATAGAAATGTGCTAGTTTT 4161 GTTTTTATATCATGTCCTTTGTACGTTGTAATATGAGCTGGCTTGGTTCAGTAAATGCCATCACCATTTCCATTGAGAAT 4241 TTAAAACTCACCAGTGTTTAATATGCAGGCTTCCAAAGGCTTATGAAAAAAATCAAGACCCTTAAATCTAGTTAATTTGC 4321 TGCTAACATGAAACTCTTTGGTTCTTTTATTTTTGCCAGATAATTAGACACACATCTAAAGCTTAGTCTTAAATGGCTTA 4401 AGTGTAGCTATTGATTAGTGCTGTTGCTAGTTCAGAAAGAAATGTTTGTGAATGGAAACAAGAATATTCAGTCCAAACTG 4481 TTGTAAGGACAGTACCTGAAAACCAGGAAACAGGATAATGGAAAAAGTCTTTTAAAGATGAAATGTTGGAGCCAACTTTC 4561 TTATAGAATTAATTGTATGTGGCTATAGAAAGCCTAATGATTGTTGCTTATTTTTGAGAGCATATTATTCTTTTATGACC 4641 ATAATCTTGCTGTTTTTCCATCTTCCAAAAGATCTTCCTTCTAATATGTATATCAGAATGTGGGTAGCCAGTCAGACAAA 4721 TTCATATTGGTTGGTAGCTTTAAAAAGTTTGTAATGTGAAGACAGGAAAGGACAAAATAGTTTGCTTTGGTGGTAGTACT 4801 CTGGTTGTTAAGCTAGGTATTTTGAGACTACTTCCCCATCACAACAACAATAAAATAATCACTCATAATCCTATCACCTG 4881 GAGACATAGCCATCGTTAATATGTTAGTGACTATACAATCATGTTTTCTTCTGTATATCCATGTATATTCTTTAAAAATG 4961 AAATTTATACTGTACCTGATCTCAAAGCTTTTTAGCTTAGTATATCTGTCATGAATTTGTAGGATGTTCCATTGCATCAG 5041 AAAACGGACAGTGATTTGATTACTTTCTAATGCCACAGATGCAGATTACATGTAGTTATTGAGAATCCTTTCGAATTCAG 5121 TGGCTTAATCATGAATGTCTAAATATTGTTGACATTAGGATGATACATGTAAATTAAAGTTACATTTGTTTAGCATAGAC 5201 AAGCTTAACATTGTAGATGTTTCTCTTCAAAAATCATCTTAAACATTTGCATTTGGAATTGTGTTAAATAGAATGTGTGA 5281 AACACTGTATTAGTAAACTTCATCACCTTTCTACTTCCTTATAGTTTGAACTTTTCAGTTTTTGTAGTTCCCAAACAGTT 5361 GCTCAATTTAGAGCAAATTAATTTAACACCTGCCAAAAAAAGGCTGCTGTTGGCTTATCAGTTGTCTTTAAATTCAAATG 5441 CTCATGTGACTTTTATCACATCAAAAAATATTTCATTAATGATTCACCTTTAGCTCTGAAAATTACCGCGTTTAGTAATT 5521 ATAGTGGGCTTATAAAAACATGCAACTCTTTTTGATAGTTATTTGAGAATTTTGGTGAAAAATATTTAGCTGAGGGCAGT 5601 ATAGAACTTATAAACCAATATATTGATATTTTTAAAACATTTTTACATATAAGTAAACTGCCATCTTTGAGCATAACTAC 5681 ATTTAAAAATAAAGCTGCATATTTTTAAATCAAGTGTTTAACAAGAATTTATATTTTTTATTTTTTAAAATTAAAAATAA 5761 TTTATATTTCCTCTGTTGCATGAGGATTCTCATCTGTGCTTATAATGGTTAGAGATTTTATTTGTGTGGAATGAAGTGAG 5841 GCTTGTAGTCATGGTTCTAGTGTTTCAGTTTGCCAAGTCTGTTTACTGCAGTGAAATTCATCAAATGTTTCAGTGTGGTT 5921 TTCTGTAGCCTATCATTTACTGGCTATTTTTTTATGTACACCTTTAGGATTTTCTGCCTACTCTATCCAGTTGTCCAAAT 6001 GATATCCTACATTTTACAAATGCCCTTTCAGTTTCTATTTTCTTTTTCCATTAAATTGCCCTCATGTCCTAATGTGCAGT 6081 TTGTAAGTGTGTGTGTGTGTGTCTGTGTGTGTGTGAATTTGATTTTCAAGAGTGCTAGACTTCCAATTTGAGAGATTAAA 6161 TAATTTAATTCAGGCAAACATTTTTCATTGGAATTTCACAGTTCATTGTAATGAAAATGTTAATCCTGGATGACCTTTGA 6241 CATACAGTAATGAATCTTGGATATTAATGAATTTGTTAGTAGCATCTTGATGTGTGTTTTAATGAGTTATTTTCAAAGTT 6321 GTGCATTAAACCAAAGTTGGCATACTGGAAGTGTTTATATCAAGTTCCATTTGGCTACTGATGGACAAAAAATAGAAATG 6401 CCTTCCTATGGAGAGTATTTTTCCTTTAAAAAATTAAAAAGGTTAATTATTTTGACTAAAAAAAAAAAAAAAAAA Target sites
Provided by authors
Predicted by miRanda
DRVs
SNPs
DRVs & SNPs
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| miRNA-target interactions (Predicted by miRanda) |
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| DRVs in gene 3'UTRs | |||||||||||||||||||||
| SNPs in gene 3'UTRs | |||||||||||||||||||||
| Experimental Support 1 for Functional miRNA-Target Interaction | |
|---|---|
| miRNA:Target | ---- |
| Validation Method |
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| Article |
- Visone R; Pallante P; Vecchione A; et al. - Oncogene, 2007
Thyroid carcinomas comprise a broad spectrum of tumors with different clinical behaviors. On the one side, there are occult papillary carcinomas (PTC), slow growing and clinically silent, and on the other side, rapidly growing anaplastic carcinomas (ATC), which are among the most lethal human neoplasms. We have analysed the microRNA (miR) profile of ATC in comparison to the normal thyroid using a microarray (miRNACHIP microarray). By this approach, we found an aberrant miR expression profile that clearly differentiates ATC from normal thyroid tissues and from PTC analysed in previous studies. In particular, a significant decrease in miR-30d, miR-125b, miR-26a and miR-30a-5p was detected in ATC in comparison to normal thyroid tissue. These results were further confirmed by northern blots, quantitative reverse transcription-PCR analyses and in situ hybridization. The overexpression of these four miRs in two human ATC-derived cell lines suggests a critical role of miR-125b and miR-26a downregulation in thyroid carcinogenesis, since a cell growth inhibition was achieved. Conversely, no effect on cell growth was observed after the overexpression of miR-30d and miR-30a-5p in the same cells. In conclusion, these data indicate a miR signature associated with ATC and suggest the miR deregulation as an important event in thyroid cell transformation.
LinkOut: [PMID: 17563749]
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| Experimental Support 2 for Functional miRNA-Target Interaction | |
|---|---|
| miRNA:Target | ---- |
| Validation Method |
|
| Conditions | NIH/3T3 , HEK293 |
| Disease | MIMAT0000082; |
| Location of target site | 3'UTR |
| Tools used in this research | TargetScan |
| Original Description (Extracted from the article) |
...
"We also show that miR-26a is frequently amplified at the DNA level in human glioma
... - Huse JT; Brennan C; Hambardzumyan D; Wee B; et al., 2009, Genes & development. |
| Article |
- Huse JT; Brennan C; Hambardzumyan D; Wee B; et al. - Genes & development, 2009
Activated oncogenic signaling is central to the development of nearly all forms of cancer, including the most common class of primary brain tumor, glioma. Research over the last two decades has revealed the particular importance of the Akt pathway, and its molecular antagonist PTEN (phosphatase and tensin homolog), in the process of gliomagenesis. Recent studies have also demonstrated that microRNAs (miRNAs) may be responsible for the modulation of cancer-implicated genes in tumors. Here we report the identification miR-26a as a direct regulator of PTEN expression. We also show that miR-26a is frequently amplified at the DNA level in human glioma, most often in association with monoallelic PTEN loss. Finally, we demonstrate that miR-26a-mediated PTEN repression in a murine glioma model both enhances de novo tumor formation and precludes loss of heterozygosity and the PTEN locus. Our results document a new epigenetic mechanism for PTEN regulation in glioma and further highlight dysregulation of Akt signaling as crucial to the development of these tumors.
LinkOut: [PMID: 19487573]
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| Experimental Support 3 for Functional miRNA-Target Interaction | |
|---|---|
| miRNA:Target | ---- |
| Validation Method |
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| Conditions | 293T |
| Disease | MIMAT0000082 |
| Location of target site | 3'UTR |
| Tools used in this research | miRanda , miRBase Target Database , TargetScan |
| Original Description (Extracted from the article) |
...
"Reporter assays in which the PTEN
... - Kim H; Huang W; Jiang X; Pennicooke B; Park et al., 2010, Proceedings of the National Academy of Sciences of the United States of America. |
| Article |
- Kim H; Huang W; Jiang X; Pennicooke B; Park et al. - Proceedings of the National Academy of Sciences of the United States of America, 2010
Using a multidimensional genomic data set on glioblastoma from The Cancer Genome Atlas, we identified hsa-miR-26a as a cooperating component of a frequently occurring amplicon that also contains CDK4 and CENTG1, two oncogenes that regulate the RB1 and PI3 kinase/AKT pathways, respectively. By integrating DNA copy number, mRNA, microRNA, and DNA methylation data, we identified functionally relevant targets of miR-26a in glioblastoma, including PTEN, RB1, and MAP3K2/MEKK2. We demonstrate that miR-26a alone can transform cells and it promotes glioblastoma cell growth in vitro and in the mouse brain by decreasing PTEN, RB1, and MAP3K2/MEKK2 protein expression, thereby increasing AKT activation, promoting proliferation, and decreasing c-JUN N-terminal kinase-dependent apoptosis. Overexpression of miR-26a in PTEN-competent and PTEN-deficient glioblastoma cells promoted tumor growth in vivo, and it further increased growth in cells overexpressing CDK4 or CENTG1. Importantly, glioblastoma patients harboring this amplification displayed markedly decreased survival. Thus, hsa-miR-26a, CDK4, and CENTG1 comprise a functionally integrated oncomir/oncogene DNA cluster that promotes aggressiveness in human cancers by cooperatively targeting the RB1, PI3K/AKT, and JNK pathways.
LinkOut: [PMID: 20080666]
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| Experimental Support 4 for Functional miRNA-Target Interaction | |
|---|---|
| miRNA:Target | ---- |
| Validation Method |
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| Location of target site | 3'UTR |
| Article |
- Inui M; Martello G; Piccolo S - Nature reviews. Molecular cell biology, 2010
MicroRNAs (miRNAs) are integral elements in the post-transcriptional control of gene expression. After the identification of hundreds of miRNAs, the challenge is now to understand their specific biological function. Signalling pathways are ideal candidates for miRNA-mediated regulation owing to the sharp dose-sensitive nature of their effects. Indeed, emerging evidence suggests that miRNAs affect the responsiveness of cells to signalling molecules such as transforming growth factor-beta, WNT, Notch and epidermal growth factor. As such, miRNAs serve as nodes of signalling networks that ensure homeostasis and regulate cancer, metastasis, fibrosis and stem cell biology.
LinkOut: [PMID: 20216554]
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| Experimental Support 5 for Functional miRNA-Target Interaction | |
|---|---|
| miRNA:Target | ---- |
| Validation Method |
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| Conditions | A549 , H661 , SK-MES-1 , BEAS-2B |
| Location of target site | 3'UTR |
| Tools used in this research | TargetScan |
| Original Description (Extracted from the article) |
...
PTEN was a direct target of miR-26a.
... - Liu B; Wu X; Liu B; Wang C; Liu Y; Zhou Q; Xu K, 2012, Biochimica et biophysica acta. |
| Article |
- Liu B; Wu X; Liu B; Wang C; Liu Y; Zhou Q; Xu K - Biochimica et biophysica acta, 2012
Lung cancer is the leading cause of cancer related death, 90% of lung cancer patients die of metastasis. Many microRNAs (miRNAs) are deregulated in cancer. They are involved in tumorigenesis and function as oncogenes or tumor suppressor genes. Recent studies show that miRNAs may be responsible for tumor metastasis. Several functional studies show that miR-26a plays an important role in carcinogenesis; however, none of these studies is related to tumor metastasis. In the present study, we investigated the effect of miR-26a on metastasis potential of lung cancer cells. Our data showed that miR-26a expression level was higher in lymph node metastasis tumor tissues than in primary tumor tissues. Ectopic expression of miR-26a dramatically enhanced lung cancer cell migration and invasion abilities. Metastasis-related genes matrix metallopeptidase 2 (MMP-2), vascular endothelial growth factor (VEGF), Twist and beta-catenin were upregulated. Phosphatase and tensin homolog (PTEN) was a direct target of miR-26a. Further mechanistic study revealed that miR-26a increased AKT phosphorylation and nuclear factor kappa B (NFkappaB) transcriptional activation. Our study demonstrated that miR-26a enhanced lung cancer cell metastasis potential via modulation of metastasis-related gene expression, and activation of AKT pathway by PTEN suppression, suggesting that miR-26a might be a potential therapeutic candidate in patients with metastatic lung cancer.
LinkOut: [PMID: 22885155]
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| Experimental Support 6 for Functional miRNA-Target Interaction | |
|---|---|
| miRNA:Target | ---- |
| Validation Method |
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| Conditions | U87 , U251 |
| Location of target site | 3'UTR |
| Tools used in this research | previous_study |
| Original Description (Extracted from the article) |
...
"Although miR-26a has been reported to be upregulated in glioblastoma multiforme (GBM)
... - Guo P; Nie Q; Lan J; Ge J; Qiu Y; Mao Q, 2013, Biochemical and biophysical research communications. |
| Article |
- Guo P; Nie Q; Lan J; Ge J; Qiu Y; Mao Q - Biochemical and biophysical research communications, 2013
The c-Myc oncogene is amplified in many tumor types. It is an important regulator of cell proliferation and has been linked to altered miRNA expression, suggesting that c-Myc-regulated miRNAs might contribute to tumor progression. Although miR-26a has been reported to be upregulated in glioblastoma multiforme (GBM), the mechanism has not been established. We have shown that ectopic expression of miR-26a influenced cell proliferation by targeting PTEN, a tumor suppressor gene that is inactivated in many common malignancies, including GBM. Our findings suggest that c-Myc modulates genes associated with oncogenesis in GBM through deregulation of miRNAs via the c-Myc-miR-26a-PTEN signaling pathway. This may be of clinical relevance.
LinkOut: [PMID: 24140063]
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| Experimental Support 7 for Functional miRNA-Target Interaction | |
|---|---|
| miRNA:Target | ---- |
| Validation Method |
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| Conditions | CLL cells |
| Location of target site | 3'UTR |
| Tools used in this research | TargetScan , mirGen , miRBase Target Database , microRNA.org |
| Original Description (Extracted from the article) |
...
"To further determine if PTEN was directly regulated by these miRNAs
... - Zou ZJ; Fan L; Wang L; Xu J; Zhang R; Tian et al., 2015, Oncotarget. |
| Article |
- Zou ZJ; Fan L; Wang L; Xu J; Zhang R; Tian et al. - Oncotarget, 2015
We previous found the expression level of PTEN was low in the chronic lymphocytic leukemia (CLL) patients. To assess the pathogenic contribution of the low expression of PTEN, we determined PTEN-regulating miRNA interference, PTEN promoter methylation and PTEN gene mutation condition in CLL. One hundred and fifty-four previously untreated CLL patients and 200 cases of healthy controls were sequenced in exons 5-9 of PTEN. None of single nucleotide polymorphism site or mutation was detected in the coding sequences of those exons. Methylation of PTEN promoter was found in one (1.33%) of the 75 patients with CLL, but none of the 25 age-matched control subjects. We found that PTEN was a potential target of miR-26a and miR-214, which had been confirmed following dual-luciferase reporter assays, reverse transcription polymerase chain reaction and Western blotting. High expression of miR-26a was associated with advanced Binet stage (P=0.012), p53 aberrations (P=0.014) and inferior time to first treatment (P=0.038), and high expression of miR-214 was only associated with p53 aberrations (P=0.041). Inhibition of miR-26a or miR-214 could induce more apoptosis in primary cultured CLL cells. These findings support miR-26a and miR-214 down-regulate expression of PTEN in CLL, but not PTEN mutation or promoter methylation.
LinkOut: [PMID: 25361012]
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| Experimental Support 8 for Non-Functional miRNA-Target Interaction | |
|---|---|
| miRNA:Target | xx |
| Validation Method |
|
| Conditions | MKN28 , AGS |
| Disease | 5728.0; gastric cancer |
| Location of target site | 3'UTR |
| Tools used in this research | TargetScan |
| Original Description (Extracted from the article) |
...
"PTEN was identified as a direct target of miR-26a//PTEN was suppressed by miR-26a through 3'-UTR
... - Ding K; Wu Z; Wang N; Wang X; Wang Y; Qian et al., 2017, Pathology, research and practice. |
| Article |
- Ding K; Wu Z; Wang N; Wang X; Wang Y; Qian et al. - Pathology, research and practice, 2017
Gastric cancer is the second leading cause of cancer-related death in the world. The exact molecular pathways in gastric cancer need for further study. We herein indicated miR-26a performed converse roles on oncogenicity in different gastric cancer cells. In gastric cancer cells MKN-28, miR-26a promoted cell proliferation, migration and invasion. However, in gastric cancer cells AGS, miR-26a reduced cell proliferation and metastasis. PTEN was identified as a direct target of miR-26a. In MKN-28 cells, PTEN was suppressed by miR-26a through 3'-UTR, and PTEN mediated miR-26a promoting oncogenicity including cell proliferation and metastasis. On the other hand, in AGS cells, the expression of PTEN was enhanced by miR-26a, and PTEN mediated miR-26a reducing oncogenicity. The mechanism in AGS cells may be the indirect regulation of PTEN by miR-26a overcame the direct targeting regulation. The model like MKN-28 cells was concordant with patients with a high level of miR-26a and a low level of PTEN and patients with a low level of miR-26a and a high level of PTEN which showed lower overall survival (OS); the model like AGS cells was concordant with patients with both high level of miR-26a and PTEN and both low level of miR-26a and PTEN which showed higher OS. These findings will facilitate a better understanding of the functions and mechanisms about miR-26a, miR-26a and PTEN are potential combined biomarkers in patients with gastric cancer.
LinkOut: [PMID: 28242043]
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| MiRNA-Target Expression Profile (TCGA) | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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449 hsa-miR-26a-5p Target Genes:
Functional analysis:
ID |
Target | Description | Validation methods |
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| Strong evidence | Less strong evidence | |||||||||||
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| MIRT000109 | HMGA2 | high mobility group AT-hook 2 |  |
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4 | 5 | ||||
| MIRT000110 | HMGA1 | high mobility group AT-hook 1 | |
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3 | 5 | |||||
| MIRT000111 | CCNE2 | cyclin E2 | |
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|
4 | 2 | ||||
| MIRT000112 | CCND2 | cyclin D2 | |
|
|
|
|
5 | 10 | |||
| MIRT001021 | CDK8 | cyclin dependent kinase 8 | |
|
2 | 2 | ||||||
| MIRT001022 | CDC6 | cell division cycle 6 | |
|
|
3 | 3 | |||||
| MIRT001039 | LIF | LIF, interleukin 6 family cytokine | |
1 | 2 | |||||||
| MIRT001095 | PTEN | phosphatase and tensin homolog | |
|
|
|
4 | 7 | ||||
| MIRT001771 | EZH2 | enhancer of zeste 2 polycomb repressive complex 2 subunit | |
|
|
|
|
5 | 11 | |||
| MIRT001772 | PLAG1 | PLAG1 zinc finger | |
|
|
3 | 2 | |||||
| MIRT002315 | SERBP1 | SERPINE1 mRNA binding protein 1 | |
|
|
3 | 3 | |||||
| MIRT002340 | SMAD1 | SMAD family member 1 | |
|
|
|
4 | 6 | ||||
| MIRT003212 | MAP3K2 | mitogen-activated protein kinase kinase kinase 2 | |
|
|
3 | 2 | |||||
| MIRT003213 | RB1 | RB transcriptional corepressor 1 | |
|
|
|
|
5 | 2 | |||
| MIRT003803 | SMAD4 | SMAD family member 4 | |
|
|
3 | 3 | |||||
| MIRT003968 | MYC | MYC proto-oncogene, bHLH transcription factor | |
|
2 | 2 | ||||||
| MIRT004338 | CTGF | connective tissue growth factor | |
|
2 | 2 | ||||||
| MIRT004339 | STRADB | STE20-related kinase adaptor beta | |
|
|
|
4 | 4 | ||||
| MIRT004615 | IFNB1 | interferon beta 1 | |
|
|
3 | 2 | |||||
| MIRT004676 | GSK3B | glycogen synthase kinase 3 beta | |
|
|
|
|
|
|
7 | 10 | |
| MIRT005587 | CPEB2 | cytoplasmic polyadenylation element binding protein 2 | |
|
|
3 | 2 | |||||
| MIRT005588 | CPEB3 | cytoplasmic polyadenylation element binding protein 3 | |
|
|
|
4 | 2 | ||||
| MIRT005589 | CPEB4 | cytoplasmic polyadenylation element binding protein 4 | |
|
|
3 | 2 | |||||
| MIRT005751 | GDAP1 | ganglioside induced differentiation associated protein 1 | |
|
|
3 | 1 | |||||
| MIRT005920 | MTDH | metadherin | |
|
|
|
|
5 | 4 | |||
| MIRT006306 | CDK6 | cyclin dependent kinase 6 | |
|
2 | 1 | ||||||
| MIRT006309 | CCNE1 | cyclin E1 | |
|
|
3 | 2 | |||||
| MIRT006389 | ESR1 | estrogen receptor 1 | |
1 | 1 | |||||||
| MIRT006711 | ABCA1 | ATP binding cassette subfamily A member 1 | |
|
2 | 1 | ||||||
| MIRT006712 | ARL4C | ADP ribosylation factor like GTPase 4C | |
|
2 | 1 | ||||||
| MIRT007177 | E2F7 | E2F transcription factor 7 | |
|
2 | 7 | ||||||
| MIRT007347 | NOS2 | nitric oxide synthase 2 | |
|
|
3 | 2 | |||||
| MIRT007374 | IL6 | interleukin 6 | |
|
2 | 1 | ||||||
| MIRT030358 | TGFBR2 | transforming growth factor beta receptor 2 | |
|
|
3 | 1 | |||||
| MIRT050053 | HIST1H4E | histone cluster 1 H4 family member e | |
1 | 1 | |||||||
| MIRT050054 | ZNF814 | zinc finger protein 814 | |
1 | 1 | |||||||
| MIRT050055 | ZNF233 | zinc finger protein 233 | |
1 | 1 | |||||||
| MIRT050056 | ABCB7 | ATP binding cassette subfamily B member 7 | |
1 | 1 | |||||||
| MIRT050057 | SCRN1 | secernin 1 | |
1 | 1 | |||||||
| MIRT050058 | NABP1 | nucleic acid binding protein 1 | |
|
2 | 8 | ||||||
| MIRT050059 | FAM20B | FAM20B, glycosaminoglycan xylosylkinase | |
1 | 1 | |||||||
| MIRT050060 | ARCN1 | archain 1 | |
1 | 1 | |||||||
| MIRT050061 | ANO3 | anoctamin 3 | |
1 | 1 | |||||||
| MIRT050062 | TFAM | transcription factor A, mitochondrial | |
1 | 1 | |||||||
| MIRT050063 | FER | FER tyrosine kinase | |
1 | 1 | |||||||
| MIRT050064 | HIAT1 | major facilitator superfamily domain containing 14A | |
1 | 1 | |||||||
| MIRT050065 | PPP1CC | protein phosphatase 1 catalytic subunit gamma | |
1 | 1 | |||||||
| MIRT050066 | SLC35B4 | solute carrier family 35 member B4 | |
1 | 1 | |||||||
| MIRT050067 | RASA1 | RAS p21 protein activator 1 | |
1 | 1 | |||||||
| MIRT050068 | COX1 | cytochrome c oxidase subunit I | |
1 | 1 | |||||||
| MIRT050069 | MSL3 | MSL complex subunit 3 | |
1 | 1 | |||||||
| MIRT050070 | GGA2 | golgi associated, gamma adaptin ear containing, ARF binding protein 2 | |
1 | 1 | |||||||
| MIRT050071 | GIT2 | GIT ArfGAP 2 | |
1 | 1 | |||||||
| MIRT050072 | DNMT1 | DNA methyltransferase 1 | |
1 | 1 | |||||||
| MIRT050073 | MFHAS1 | malignant fibrous histiocytoma amplified sequence 1 | |
1 | 1 | |||||||
| MIRT050074 | UBA2 | ubiquitin like modifier activating enzyme 2 | |
1 | 1 | |||||||
| MIRT050075 | DCAF7 | DDB1 and CUL4 associated factor 7 | |
1 | 1 | |||||||
| MIRT050076 | MTRF1 | mitochondrial translation release factor 1 | |
1 | 1 | |||||||
| MIRT050077 | WBSCR16 | RCC1 like | |
1 | 1 | |||||||
| MIRT050078 | NUAK1 | NUAK family kinase 1 | |
1 | 1 | |||||||
| MIRT050079 | TUT1 | terminal uridylyl transferase 1, U6 snRNA-specific | |
1 | 1 | |||||||
| MIRT050080 | PNMA2 | paraneoplastic Ma antigen 2 | |
1 | 1 | |||||||
| MIRT050081 | ACTL8 | actin like 8 | |
1 | 1 | |||||||
| MIRT050082 | HSPA8 | heat shock protein family A (Hsp70) member 8 | |
1 | 1 | |||||||
| MIRT050083 | DHX15 | DEAH-box helicase 15 | |
1 | 1 | |||||||
| MIRT050084 | TCP1 | t-complex 1 | |
1 | 1 | |||||||
| MIRT050085 | SLC25A5 | solute carrier family 25 member 5 | |
1 | 1 | |||||||
| MIRT050086 | LSM14A | LSM14A, mRNA processing body assembly factor | |
1 | 1 | |||||||
| MIRT050087 | CAMKV | CaM kinase like vesicle associated | |
1 | 1 | |||||||
| MIRT050088 | ALG10B | ALG10B, alpha-1,2-glucosyltransferase | |
1 | 1 | |||||||
| MIRT050089 | TYW1 | tRNA-yW synthesizing protein 1 homolog | |
1 | 1 | |||||||
| MIRT050090 | RPL13A | ribosomal protein L13a | |
1 | 1 | |||||||
| MIRT050091 | AGO1 | argonaute 1, RISC catalytic component | |
1 | 1 | |||||||
| MIRT050092 | TXLNG | taxilin gamma | |
1 | 1 | |||||||
| MIRT050093 | RAB18 | RAB18, member RAS oncogene family | |
1 | 1 | |||||||
| MIRT050094 | RPS27A | ribosomal protein S27a | |
1 | 1 | |||||||
| MIRT050095 | RPS26 | ribosomal protein S26 | |
1 | 1 | |||||||
| MIRT050096 | PIKFYVE | phosphoinositide kinase, FYVE-type zinc finger containing | |
1 | 1 | |||||||
| MIRT050097 | TP53INP1 | tumor protein p53 inducible nuclear protein 1 | |
1 | 1 | |||||||
| MIRT050098 | ZNF703 | zinc finger protein 703 | |
1 | 1 | |||||||
| MIRT050099 | MTRF1L | mitochondrial translational release factor 1 like | |
1 | 1 | |||||||
| MIRT050100 | ZNF506 | zinc finger protein 506 | |
1 | 1 | |||||||
| MIRT050101 | KCTD5 | potassium channel tetramerization domain containing 5 | |
1 | 1 | |||||||
| MIRT050102 | CTC1 | CST telomere replication complex component 1 | |
1 | 1 | |||||||
| MIRT050103 | TKT | transketolase | |
1 | 1 | |||||||
| MIRT050104 | LYST | lysosomal trafficking regulator | |
1 | 1 | |||||||
| MIRT050105 | FAM134A | reticulophagy regulator family member 2 | |
1 | 1 | |||||||
| MIRT050106 | NKX2-5 | NK2 homeobox 5 | |
1 | 1 | |||||||
| MIRT050107 | AURKAIP1 | aurora kinase A interacting protein 1 | |
1 | 1 | |||||||
| MIRT050108 | ATP1A1 | ATPase Na+/K+ transporting subunit alpha 1 | |
1 | 1 | |||||||
| MIRT050109 | COASY | Coenzyme A synthase | |
1 | 1 | |||||||
| MIRT050110 | CTR9 | CTR9 homolog, Paf1/RNA polymerase II complex component | |
1 | 1 | |||||||
| MIRT050111 | COX3 | cytochrome c oxidase III | |
1 | 1 | |||||||
| MIRT050112 | ELOVL6 | ELOVL fatty acid elongase 6 | |
1 | 1 | |||||||
| MIRT050113 | PIGT | phosphatidylinositol glycan anchor biosynthesis class T | |
1 | 1 | |||||||
| MIRT050114 | TMCC3 | transmembrane and coiled-coil domain family 3 | |
1 | 1 | |||||||
| MIRT050115 | ARHGEF1 | Rho guanine nucleotide exchange factor 1 | |
1 | 1 | |||||||
| MIRT050116 | SHC2 | SHC adaptor protein 2 | |
1 | 1 | |||||||
| MIRT050117 | PSMA3 | proteasome subunit alpha 3 | |
1 | 1 | |||||||
| MIRT050118 | PTTG1 | pituitary tumor-transforming 1 | |
1 | 1 | |||||||
| MIRT050119 | RPS24 | ribosomal protein S24 | |
1 | 1 | |||||||
| MIRT050120 | SPTBN1 | spectrin beta, non-erythrocytic 1 | |
1 | 1 | |||||||
| MIRT050121 | UBTF | upstream binding transcription factor, RNA polymerase I | |
1 | 1 | |||||||
| MIRT050122 | BTBD3 | BTB domain containing 3 | |
1 | 1 | |||||||
| MIRT050123 | AHR | aryl hydrocarbon receptor | |
1 | 1 | |||||||
| MIRT050124 | EEF1B2 | eukaryotic translation elongation factor 1 beta 2 | |
1 | 1 | |||||||
| MIRT050125 | MRPL51 | mitochondrial ribosomal protein L51 | |
1 | 1 | |||||||
| MIRT050126 | SETD2 | SET domain containing 2 | |
1 | 1 | |||||||
| MIRT050127 | LRP6 | LDL receptor related protein 6 | |
1 | 1 | |||||||
| MIRT050128 | RHOBTB1 | Rho related BTB domain containing 1 | |
1 | 1 | |||||||
| MIRT050129 | HIST1H4J | histone cluster 1 H4 family member j | |
1 | 1 | |||||||
| MIRT050130 | MYO10 | myosin X | ||||||||||