| 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 |
| 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 |
| 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 |
| 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 |
| 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 |
| 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 |
| 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 |
| 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 |
| 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 |
| 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 |
| 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 |
| 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 |
| Mir1 | — | miR-1 is associated with stem cell differentiation in mouse and human ESCs [18371447]. | House mouse |
| 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 |
| 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 |
| 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 |
| Mir133 | — | miR-133 is associated with stem cell differentiation in mouse and human ESCs [18371447]. | House mouse |
| 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 |
| — | — | ENSRNOG00000044316 is transcriptional downregulated in the cerebral cortex at the age 28 months under different longevity conditions such as under dietary restriction (DR) as well as in feeding switch regimens that result in extended lifespan, like early age switch to DR as well as the reverse switch under the influence of the DR-mimetic α-lipoic acid (i.e. DR switched to ad libitum+ lipoic acid) [Shona et al. 2013]. | Norway rat |
| — | — | ENSRNOG00000044070 is transcriptional upregulated in the cerebral cortex at the age 28 months under different longevity conditions such as under dietary restriction (DR) as well as in feeding switch regimens that result in extended lifespan, like early age switch to DR as well as the reverse switch under the influence of the DR-mimetic α-lipoic acid (i.e. DR switched to ad libitum+ lipoic acid) [Shona et al. 2013]. | Norway rat |
| 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 |
