| 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 |
| 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 |
| 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 |
| mir-34 | — | mir-34 loss triggers a gene expression profile of accelerated brain aging, late-onset brain degeneration and catastrophic decline in survival, while mir-34 upregulation extends median lifespan and mitigated neurodegeneration induced by polyglutamine. | Fruit fly |
| 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 |
| mir-58 | — | mir-58(n4640) mutation decreases the mean lifespan by 20% [22482727]. | Nematode |
| Mir98 | microRNA mir-98 | miR-98-3p is the only miRNA significantly differentially expressed (upregulated) under DR and LA (lipoic acid; a DR-mimetic) treatment. Across mouse, rat and human predicted targets of miR-98-3p include the glutamate receptors, calcium transporters, histones and histone acetyltransferase/deacetylases.
miR-89-3p is expressed at a low level and is highly conserved in rat, mouse, human and anplis lizard. Mir-98 precursor is located on the X-chromosome. In the rat, mouse and human genome it overlaps an E3 ubiquitin ligase HUWE which is involved in regulation of apoptosis, regulation of neural differentiation and proliferation, DNA damage repair [Shona et al. 2013].
miR-98 expression is significantly decreased in the adventitia and endomembrane ath different degrees in Goto-Kakizaki rat, a model of type 2 diabetes. miR-98 targets TRB2 which is increased in expression in this model of type 2 diabetes. TRB2 phosphorylates Akt [22012613].
The mouse ortholog of Mir98 may by associated with the germline [16766679]. | Norway rat |
| MIR106A | microRNA 106A | MIR106A is downregulated in senescent cells as it has a good correlation with p21 transcription, while p53 represses mir17-92 cluster [20437201; 20089119]. | Human |
| MIR145 | microRNA 145 | MIR145 is a tumor suppressor that acts by inhibiting IRS-1 in human colon cancer cells. It also targets IGFR1 [17827156; 19391107]. It decreases cell migration in gliomas by targeting CTGF, metastasis and migration-promoting gene. MIR145 is downregulated in astrocytic tumors and oligodendrogliomas [23390502;
23577178]. | Human |
| miR148a | microRNA 148a | miR148a belongs to miR148-152 cluster and acts as a tumor-suppressor in different types of cancer. MiR148a expression is suppressed more than 4-fold in gastric cancer. An inverse correlation has been observed between miR148a expression and lymph node metastasis in gastric cancer. Mir148a suppresses migratory abilities of cancer cells and metastasis formation by downregulating the oncogene ROCK1 expression [21994419]. miR148a is downregulated in pancreatic ductal adenocarcinoma (PDAC). it has been shown that miR148a directly targets the 3'UTR region of CDC25B mRNA. CDC25B is a phosphatase that, by activating a cyclin-CDK complex, initiates mitosis, therefore CDC25B suppression by miR148a could have a tumor-suppressor effect on PDAC. [21709669] | Human |
| miR148b | microRNA 148b | Mir148b belongs to mir148/152 cluster and acts as a tumor-suppressor in certain types of cancer. As a result of a study of miR148b expression in gastric cancer it has been determined that in 62 percent of cases, in tumor tissue miRNA was downregulated compared to adjacent non-tumor tissue. MiR148b suppresses tumorigenecity by targeting CCKBR, whose action is to mediate the function of gastrin, which has proliferative effects. |21205300] In addition, while miR148b is downregulated in pancreatic cancer tissues, its overexpression inhibits invasion and increases chemosensitivity [23171948]. | Human |
| 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 |
| 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 |
| 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 | 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 |
| 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 |
| mir-14 | mir-14 stem loop | Mutating mir-14 decreases lifespan in both sexes. mir-14 reduces the mean and maximum lifespan of females by 55 and 36%, respectively, while those of males is reduced by 29 and 21%, respectively [12725740].
| Fruit fly |
| mir-238 | — | Mutating mir-238 decreases mean and maximum lifespan by 18 and 24% [21129974]. mir-238(n4112) mutation decreases mean lifespan by 20% [22482727]. | Nematode |
| mir-239 | — | Mutating mir-239 increases mean and maximum lifespan by 12 and 36%, respectively, whereas overexpressing mir-239 decreases mean and maximum lifespan by 13 and 17 - 33%, respectively [21129974]. | Nematode |
