MicroRNAs as a novel cellular senescence regulator

Liu, Fengjiao; Wen, Tie; Liu, Ling

doi:10.1016/j.arr.2011.06.001

Cited by 46 publications

(33 citation statements)

References 131 publications

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“…The main senescence pathways associated with miRNAs are the p53/p21 and p16/Rb pathways (15). Especially, many studies have focused on the miR-34a/SIRT1/p53 interaction (17).…”

mentioning

confidence: 99%

Anti-oncogenic MicroRNA-203 Induces Senescence by Targeting E2F3 Protein in Human Melanoma Cells

Noguchi

Mori

Otsuka³

et al. 2012

Journal of Biological Chemistry

103

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Background: MicroRNA-203 is down-regulated, and its exogenous expression inhibits cell growth in human melanoma cells. Results: MicroRNA-203 induced senescence by cell cycle arrest through targeting E2F3. Conclusion: MicroRNA-203 is a novel senescence-associated microRNA in melanoma cells. Significance: This study has revealed the relationship between senescence and carcinogenesis in melanoma cells with respect to dysregulation of anti-oncogenic microRNA-203.

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“…The main senescence pathways associated with miRNAs are the p53/p21 and p16/Rb pathways (15). Especially, many studies have focused on the miR-34a/SIRT1/p53 interaction (17).…”

mentioning

confidence: 99%

Anti-oncogenic MicroRNA-203 Induces Senescence by Targeting E2F3 Protein in Human Melanoma Cells

Noguchi

Mori

Otsuka³

et al. 2012

Journal of Biological Chemistry

103

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“…Recently, miRNAs, which are important regulatory factors due to their potent regulation of target genes, have been shown to be novel modulators of senescence, aging, and longevity (Grillari and Grillari-Voglauer 2010;Liu et al 2011). However, thus far, no direct target of miR-543 and miR-590-3p has been reported, and only one target, hnRNP-A1, has been predicted for miR-590-3p in Alzheimer's disease patients (Villa et al 2011).…”

Section: Discussionmentioning

confidence: 99%

“…MicroRNAs (miRNAs) are small, non-coding RNAs that are ∼22 nucleotides in length and are known to regulate genes that are important for maintaining clonogenicity and adipogenic differentiation potential or for inducing cellular senescence through the repression of target mRNA translation via complementary binding to the 3′ untranslated region (UTR) (Bonifacio and Jarstfer 2010;Liu et al 2011;Martinez et al 2011;Yi et al 2008). The let-7 family of miRNAs inhibits KRAS, HMGA2, and c-MYC expression and induces replicative cellular senescence (Chivukula and Mendell 2008;Grillari and Grillari-Voglauer 2010).…”

mentioning

confidence: 99%

miR-543 and miR-590-3p regulate human mesenchymal stem cell aging via direct targeting of AIMP3/p18

Lee

Ryu

et al. 2014

AGE

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A b s t r a c t P r e v i o u s l y, A I M P 3 ( a m i n o a c y ltRNAsynthetase-interacting multifunctional protein-3) was shown to be involved in the macromolecular tRNA synthetase complex or to act as a tumor suppressor. In this study, we report a novel role of AIMP3/p18 in the cellular aging of human mesenchymal stem cells (hMSCs). We found that AIMP3/p18 expression significantly increased in senescent hMSCs and in aged mouse bone marrow-derived MSCs (mBM-MSCs). AIMP3/p18 overexpression is sufficient to induce the cellular senescence phenotypes with compromised clonogenicity and adipogenic differentiation potential. To identify the upstream regulators of AIMP3/p18 during senescence, we screened for potential epigenetic regulators and for miRNAs. We found that the levels of miR-543 and miR-590-3p significantly decreased under senescence-inducing conditions, whereas the AIMP3/p18 protein levels increased. We demonstrate for the first time that miR-543 and miR-590-3p are able to decrease AIMP3/p18 expression levels through direct AGE (2014) binding to the AIMP/p18 transcripts, which further compromised the induction of the senescence phenotype. Taken together, our data demonstrate that AIMP3/ p18 regulates cellular aging in hMSCs possibly through miR-543 and miR-590-3p.

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“…[77]). Conversely, several studies evidence that members of the miR-34 family are direct transactivational targets of p53 [78][79][80][81].…”

Section: Micrornas and Senescencementioning

confidence: 99%

From experimental design to functional gene networks: DNA microarray contribution to skin ageing research

Benech

Patatian

2014

Intern J of Cosmetic Sci

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SynopsisThere is no doubt that the DNA microarray-based technology contributed to increase our knowledge of a wide range of processes. However, integrating genes into functional networks, rather than terms describing generic characteristics, remains an important challenge. The highly context-dependent function of a given gene and feedback mechanisms complexify greatly the interpretation of the data. Moreover, it is difficult to determine whether changes in gene expression are the result or the cause of pathologies or physiological events. In both cases, the difficulty relies on the involvement of processes that, at an early stage, can be protective and later on, deleterious because of their runaway. Each individual cell has its own transcription profile that determines its behaviour and its relationships with its neighbours. This is particularly true when a mechanism such as cell cycle is concerned. Another issue concerns the analyses from samples of different donors. Whereas the statistical tools lead to determine common features among groups, they tend to smooth the overall data and consequently, the selected values represent the 'tip of the iceberg'. There is a significant overlap in the set of genes identified in the different studies on skin ageing processes described in the present review. The reason of this overlap is because most of these genes belong to the basic machinery controlling cell growth and arrest. To get a more full picture of these processes, a hard work has still to be done to determine the precise mechanisms conferring the cell type specificity of ageing. Integrative biology applied to the huge amount of existing microarray data should fulfil gaps, through the characterization of additional actors accounting for the activation of specific signalling pathways at crossing points. Furthermore, computational tools have to be developed taking into account that expression values among similar groups may not vary 'by chance' but may reflect, along with other subtle changes, specific features of one given donor. Through a better stratification, these tools will allow to recover genes from the 'bottom of the iceberg'. Identifying these genes should contribute to understand how skin ages among individuals, thus paving the way for personalized skin care.R esum e Il ne fait aucun doute que la technologie de puces a ADN a contribu e, via l'identification de centaines de g enes, a accroître nos connaissances dans de nombreux processus, incluant le vieillissement. Cependant, int egrer des g enes dans des r eseaux fonctionnels, plutôt que de d efinir des termes d ecrivant des caract eristiques g en eriques, reste un d efi important. La fonction d'un g ene donn e qui peut varier selon le contexte et les m ecanismes de r etrocontrôle complexifient grandement l'interpr etation des donn ees de puces. De plus, il est difficile de d eterminer si les modifications d'expression des g enes sont le r esultat ou la cause d'une pathologie ou d'un ev enement physiologique tel que le vieillissement. Dans les deux cas, ...

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MicroRNAs as a novel cellular senescence regulator

Cited by 46 publications

References 131 publications

Anti-oncogenic MicroRNA-203 Induces Senescence by Targeting E2F3 Protein in Human Melanoma Cells

Anti-oncogenic MicroRNA-203 Induces Senescence by Targeting E2F3 Protein in Human Melanoma Cells

miR-543 and miR-590-3p regulate human mesenchymal stem cell aging via direct targeting of AIMP3/p18

From experimental design to functional gene networks: DNA microarray contribution to skin ageing research

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