| MIR34C | microRNA 34c | — | Human |
| hsa-let-7c | microRNA let-7c | let-7c is downregulated in prostate cancer, which increases cell proliferation [22479342]. More specifically, let-7c is a regulator of androgen receptor (AR), which plays a role in the development of prostate cancer [22128178]. | Human |
| lin-4 | abnormal cell LINeage 4 | A loss-of-function mutation in lin-4 shortens lifespan and accelerated tissue ageing while overexpressing lin-4 extends lifespan by redarding aging [16373574].
lin-4 is regulated by DAF-16 in L1 arrest. | Nematode |
| hsa-let-7a | microRNA let-7a | A tumor-suppressor downregulated in different types of cancer. Let-7a binds to 3'-UTR region of RAB40C, thus leading to a decrease in cell proliferation and an increase of G1 arrest in human gastric carcinomas [20809749, 21349817]. In human breast cancer, evidence suggests that members of let-7 family inhibit breast cancer cell migration by targeting genes responsible for actin dynamics [23339187]. Moreover, let-7a directly targets CCR7, a receptor that promotes invasiveness of cancer cells [23335963] | Human |
| mir-277 | — | Constitutive miR-277 expression shortens lifespan and synthetically lethal with reduced insulin signaling, indicating that metabolic control underlies this phenotype. Transgenic inhibition with a miRNA sponge construct also shortens lifespan [23669073].
miR-277 is downregulated during adult life [23669073].
mir-277 controls branched-chain amino acid catabolism and as a result it can modulate the activity of TOR kinase [23669073]. | Fruit fly |
| miR-214 | microRNA 214 | Expression increases with age in mouse liver. The miRNA downregulates detoxification and regeneration genes, which may contribute to aging [18561983]. | House mouse |
| 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 |
| hsa-let-7f | — | hsa-let-7f is significantly upregulated in senescent human mesenchymal stem cells (hMSCs) when compared to early passage hMSC [18493317]. | Human |
| MIRC29 | microRNA 29c | hsa-miR-29c is significantly upregulated in senescent human mesenchymal stem cells (hMSCs) when compared to early passage hMSC [18493317]. | 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 |
| MIR499 | microRNA-449 | hsa-miR-499 is significantly upregulated in senescent human mesenchymal stem cells (hMSCs) when compared to early passage hMSC [18493317]. | Human |
| hsa-let-7b | microRNA let-7b | Let-7b, a member of the let-7 group, appears to be a tumor-suppressor. In acute lymphoblastic leukemia, let-7b is severely downregulated and its overexpression inhibits cancer cells growth [22918121]. In melanoma cells, the miRNA downregulates the expression of cell cycle regulators such as cyclin D1, D3, and A and Cdk4, which inhibits cell cycle progression. [18379589] | Human |
| mir-71 | — | Loss and gain-of-function of mir-71 decreases and increases lifespan, respectively [21129974]. mir-71 mutants have a reduced lifespan with 40% decrease in mean lifespan, while extra copies of mir-71 extend the lifespan with an increase in lifespan by 15 - 25% [22482727],
Loss of mir-71 function suppresses the long lifespan of glp-1(e2141) mutants [22482727],
During adulthood mir-71 is strongly expressed in the intestine, body wall muscles and neurons. mir-71 is upregulated in aging adults [22482727], | Nematode |
| mir-124 | — | Loss of mir-124 increases reactive oxygen species formation and accumulation of the aging marker lipofuscin, reduces whole body ATP levels and results in reduction in lifespan [23075628].
Supplementation of vitamin C normalizes the reduced median lifespan of mir-124 mutants [23075628].
The expression of the conserved mir-124 in whole wrn-1 mutants (which premature age) is significantly reduced [23075628]. | Nematode |
| Mir1 | — | miR-1 is associated with stem cell differentiation in mouse and human ESCs [18371447]. | House mouse |
| Mir133 | — | miR-133 is associated with stem cell differentiation in mouse and human ESCs [18371447]. | House mouse |
| MIR146B | microRNA 146b | miR-146a/b is significantly elevated during senescence as a compensatory response to restrain inflammation via the suppression of IL-6 and IL-8 secretion and downregulation of IRAK1 (component of IL-1 receptor signaling). Ectopic expression of miR-146a/b in primary fibroblasts suppresses IL-6 and IL-8 secretion and downregulation of IRAK1 [20148189]. | Human |
| MIR146A | microRNA 146a | miR-146a/b is significantly elevated during senescence as a compensatory response to restrain inflammation via the suppression of IL-6 and IL-8 secretion and downregulation of IRAK1 (component of IL-1 receptor signaling). Ectopic expression of miR-146a/b in primary fibroblasts suppresses IL-6 and IL-8 secretion and downregulation of IRAK1 [20148189]. | 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 |
| 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 |
