| miR152 | microRNA 152 | MiR152 belongs to miR148/152 cluster and can act as a tumor-suppressor. In ovarian cancer, miR152 suppresses DNMT1 directly and inhibits proliferation of cancer cells. [23318422] The miRNA is downregulated in ovarian cancer cells lines and its downregulation may lead to deregulation of cell proliferation in ovarian cancer. [21971665]
| Human |
| MIR155 | microRNA 155 | mir-155 is significantly overexpressed in human breast cancer while targeting the miRNA could induce apoptosis and cell cycle arrest as well as inhibit cell growth. [18719391]. Mir155 acts by repressing socs1, a tumor suppressor. In addition, inflammatory signals may activate miR155, thus suggesting that the miRNA serves as a link between inflammation and malignancy formation [20354188]. It is also upregulated in lung cancer and acts an oncogene by targeting Apaf1 and thus reducing apoptosis rate [22996741]. Inhibition of mir-155 radiosensitizes cancer cells [22027557]. | Human |
| MIR15A | microRNA 15a | MIR15A is a tumor-suppressor downregulated in different types of cancers. In chronic lymphocytic leukemia (CLL) it is downregulated in 68% of cases [12434020]. MIR15A may post-transcriptionally downregulate the expression of Bcl2, thus inducing apoptosis. Therefore, inactivation of MIR15A and MIR16-1 in CLL lymphocytes results in a reduced apoptosis rate [16166262].
In prostate cancer, MIR15A and MIR16-1 are downregulated, which results in decreased repression of FGF-2, thus promoting tumor expansion and invasiveness [21532615].
MIR15A and MIR16-1 are also downregulated in pituitary adenomas as thier expression exhibits an inverse correlation with tumor diameter, therefore possible influence on tumor growth [15648093]. | Human |
| MIR16-1 | microRNA16-1 | MIR16-1 is a tumor-suppressor downregulated in different types of cancers. In chronic lymphocytic leukemia (CLL) it is downregulated in 68% of cases [12434020]. MIR16-1 may post-transcriptionally downregulate the expression of Bcl2, thus inducing apoptosis. Therefore, inactivation of MIR15A and MIR16-1 in CLL lymphocytes results in a reduced apoptosis rate [16166262].
In prostate cancer, MIR15A and MIR16-1 are downregulated, which results in decreased repression of FGF-2, thus promoting tumor expansion and invasiveness [21532615].
MIR15A and MIR16-1 are also downregulated in pituitary adenomas as thier expression exhibits an inverse correlation with tumor diameter, therefore possible influence on tumor growth [15648093]. | Human |
| miR17 | microRNA 17 | miR17 is downregulated in senescent cells and has a good correlation with p21 transcription, while p53 represses mir17-92 cluster [20437201; 20089119] | Human |
| MIR20A | microRNA 20a | Overexpression of MiR-20a in mouse embryonic fibroblasts induces senescence by lowering Lrf (a transcriptional repressor of the Mdm2 inhibitor p19ARF [15662416; 9529248]) protein levels and in turn increasing p19ARF levels [18596985]. | House mouse |
| MIR21 | MIRN21; hsa-mir-21; miR-21; miRNA21 | MIR21 is the most highly expressed microRNA gene in octogenarians and centenarians. MIR21 expression is higher under cardiovascular diseases and lower in centenarian offspring. MIR21 is correlated with C-reactive protein and fibrinogen levels. TGF-βR2 mRNA, a MIR21 target, exhibits the highest expression in leukocytes form a subset of octogenarians. MIR-21 may be a biomarker of inflammation [23041385]. | Human |
| MIR217 | microRNA 217 | MIR217 (alias hsa-miR-217) is significantly upregulated in senescent human mesenchymal stem cells (hMSCs) when compared to early passage hMSC, but overall had very low expression levels [18493317]. | Human |
| miR221 | microRNA 221 | miR221 and miR222 downregulate PTEN, a major tumor suppressor and TIMP3, which induces activation of caspases 8 and 9 [19962668]. Thus miR221 and miR222 enhance tumorigenecity in cell lung cancer, gastric cancer and hepatocarcinoma cells [20618998] | Human |
| miR222 | microRNA 222 | miR221 and miR222 downregulate PTEN, a major tumor suppressor and TIMP3, which induces activation of caspases 8 and 9 [19962668]. Thus miR221 and miR222 enhance tumorigenecity in cell lung cancer, gastric cancer and hepatocarcinoma cells [20618998]. | Human |
| Mir27a | MicroRNA 27a | In Ames dwarf mice (which displays delayed Aging), Mir27a expression is significantly higher than in control mice. Mir27a may be responsible for delayed Aging in dwarf mice: it suppresses the expression of ODC1 and SRM, which in turn suppresses polyamine synthesis in dwarf mice liver. Part of the ability of dwarf mice to suppress or avoid tumor or Cancer growth may be attributed to the decreased Polyamine biosynthesis. [19878148] | House mouse |
| MIR27A | microRNA 27a | MIR27A can be both a tumor-suppressor and an oncogene. For instance, the expression of miR-27a is significantly lower in acute leukemia compared to normal cells. It has been shown that miRNA-27a inhibits cell growth and promotes apoptosis by targeting 14-3-3θ, a member of 14-3-3 family of anti-apoptotic proteins. [23236401]. Therefore, it acts as a tumor-suppressor in leukemia. However, in gastric cancer mir-27a acts as an oncogene by targeting inhibiting and thus promoting cancer cell growth [18789835]. | Human |
| MIR29A | microRNA 29a | miR-29a reduces the amount of methylation and upregulates a long non-coding RNA form a region called MEG3 that is responsible for inducing apoptotic pathway. Thus reducing tumorgensis in non-malignant hepatocytes [21625215].
| Human |
| MIR34A | microRNA 34a | mir-34 family, particularly miR-34a, as downstream effectors of p53 involved in cell cycle [17656095], leads to cell cycle arrest, increased expression of Beta-galactosidase [17554337] and downregulation of E3F family target genes [17875987]. MDM2 inhibiting drug Nutlin-3, leads to p53 activation, induced up-regulation of primarily miR-34a and later miR-34b and miR-34c [18451145]. | Human |
| Mir34a | microRNA mir-34a | Increases in aging rat liver, which suppresses the expression of such proteins as Sirt1 and Mgst1, resulting in dysfunction of oxidative stress defense and regulation [21216258] | Norway rat |
| MIR34B | microRNA 34b | mir-34 family, particularly miR-34a, as downstream effectors of p53 involved in cell cycle [17656095], leads to cell cycle arrest, increased expression of Beta-galactosidase [17554337] and downregulation of E3F family target genes [17875987]. MDM2 inhibiting drug Nutlin-3, leads to p53 activation, induced up-regulation of primarily miR-34a and later miR-34b and miR-34c [18451145]. | Human |
| MIR34C | microRNA 34c | — | Human |
| MIR369 | microRNA 369 | hsa-miR-369-5p is significantly upregulated in senescent human mesenchymal stem cells (hMSCs) when compared to early passage hMSC [18493317]. | Human |
| MIR371A | microRNA 371a | hsa-miR-371 is significantly upregulated in senescent human mesenchymal stem cells (hMSCs) when compared to early passage hMSC [18493317]. | Human |
| MIR372 | microRNA 372 | miR-372 expression is able to bypass RAS-induced senescence in presence of wild-type p53 [16564011]. | Human |
| MIR373 | microRNA 373 | miR-373 expression is able to bypass RAS-induced senescence in presence of wild-type p53 [16564011]. | Human |
| Mir489 | microRNA 489 | Mir489 is maintaining adult stem cells in quiescence phase. Inhibition of miR489 is sufficient to make murine satellite muscle cells exit the quiescence phase and enter the cell cycle through downregulation of the oncogene Dek [22358842]. | House mouse |
| MIR499 | microRNA-449 | hsa-miR-499 is significantly upregulated in senescent human mesenchymal stem cells (hMSCs) when compared to early passage hMSC [18493317]. | Human |
| Mir669c | microRNA 669c | Expression increases with age in mouse liver. The miRNA downregulates detoxification and regeneration genes, which may contribute to aging [18561983]. | House mouse |
| Mir93 | microRNA mir-93 | Increases in Aging rat Liver, which suppresses the expression of such proteins as Sirt1 and Mgst1, resulting in dysfunction of oxidative stress defense and regulation [21216258] | Norway rat |
