Factors

We need to know every factor which determines lifespan.

Lifespan factors often but not always originate from defined genetic elements. They are not just genes, by definition they can be anything for which a Classifications schema can be build for that is related to the regulation of lifespan, such entities may include Single-Nucleotide Polymorphism, transcript variants, proteins and their complexes, compounds (i.e. small molecules like metabolites and drugs), etc. A factor should be based on a defined molecular entity or genomic position and been classified. It shall be highly flexible and scalable Concept.

While individual lifespan factors within each species or precise defined molecular entities will be captured within the Lifespan App, Data Entries of the Data App may summarize for instance the relevance of each factor class (e.g. homologous group; chemical derivate of related structure and properties, etc.) as well as draw overall conclusions. o

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  • Species: + -
  • symbol name observation species
    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
    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-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
    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
    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
    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
    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
    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
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    • 25 of 27 factors
    Factors are an extension of GenAge and GenDR.

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