Activation of p53 by MEG3 Non-coding RNA

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Abstract

MEG3 is a maternally expressed imprinted gene suggested to function as a non-coding RNA. Our previous studies suggest that MEG3 has a function of tumor suppression. The tumor suppressor p53 plays a central role in tumor suppression and mediates the functions of many other tumor suppressors. Therefore, we hypothesized that MEG3 functions through activation of p53. We found that transfection of expression constructs for MEG3 and its isoforms results in a significant increase in p53 protein levels and dramatically stimulates p53-dependent transcription from a p53-responsive promoter. Using this as the functional assay, we demonstrated that the open reading frames encoded by MEG3 transcripts are not required for MEG3 function, and the folding of MEG3 RNA is critical to its function, supporting the concept that MEG3 functions as a non-coding RNA. We further found that MEG3 stimulates expression of the growth differentiation factor 15 (GDF15) by enhancing p53 binding to the GDF15 gene promoter. Interestingly, MEG3 does not stimulate p21CIP1 expression, suggesting that MEG3 can regulate the specificity of p53 transcriptional activation. p53 degradation is mainly mediated by the mouse double minute 2 homolog (MDM2). We found that MDM2 levels were down-regulated in cells transfected with MEG3, suggesting that MDM2 suppression contributes at least in part to p53 accumulation induced by MEG3. Finally, we found that MEG3 is able to inhibit cell proliferation in the absence of p53. These data suggest that MEG3 non-coding RNA may function as a tumor suppressor, whose action is mediated by both p53-dependent and p53-independent pathways. MEG3 is a maternally expressed imprinted gene suggested to function as a non-coding RNA. Our previous studies suggest that MEG3 has a function of tumor suppression. The tumor suppressor p53 plays a central role in tumor suppression and mediates the functions of many other tumor suppressors. Therefore, we hypothesized that MEG3 functions through activation of p53. We found that transfection of expression constructs for MEG3 and its isoforms results in a significant increase in p53 protein levels and dramatically stimulates p53-dependent transcription from a p53-responsive promoter. Using this as the functional assay, we demonstrated that the open reading frames encoded by MEG3 transcripts are not required for MEG3 function, and the folding of MEG3 RNA is critical to its function, supporting the concept that MEG3 functions as a non-coding RNA. We further found that MEG3 stimulates expression of the growth differentiation factor 15 (GDF15) by enhancing p53 binding to the GDF15 gene promoter. Interestingly, MEG3 does not stimulate p21CIP1 expression, suggesting that MEG3 can regulate the specificity of p53 transcriptional activation. p53 degradation is mainly mediated by the mouse double minute 2 homolog (MDM2). We found that MDM2 levels were down-regulated in cells transfected with MEG3, suggesting that MDM2 suppression contributes at least in part to p53 accumulation induced by MEG3. Finally, we found that MEG3 is able to inhibit cell proliferation in the absence of p53. These data suggest that MEG3 non-coding RNA may function as a tumor suppressor, whose action is mediated by both p53-dependent and p53-independent pathways. RNAs that do not encode any proteins and function at the RNA level are non-coding RNAs (ncRNAs). 3The abbreviations used are: ncRNAnon-coding RNABrdUrdbromodeoxyuridineChIPchromatin immunoprecipitationCMVcytomegalovirusGDF15growth differentiation factor 15ORFopen reading framewtwild typeMEG3maternally expressed gene 3rRNAribosomal RNAGFPgreen fluorescent proteinTRITCtetramethylrhodamine isothiocyanateLIlabeling indexAct Dactinomycin DE3ubiquitin-protein isopeptide ligaseMDM2mouse double minute 2 homolog In recent years, emerging evidence indicates that they play important roles in regulating cellular and biological functions (1Mattick J.S. Makunin I.V. Hum. Mol. Genet. 2006; 15: R17-R29Crossref PubMed Scopus (1853) Google Scholar, 2Pang K.C. Frith M.C. Mattick J.S. Trends Genet. 2006; 22: 1-5Abstract Full Text Full Text PDF PubMed Scopus (506) Google Scholar). Besides the well known transfer RNAs and ribosomal RNAs, ncRNAs can be categorized into small nuclear RNAs, small nucleolar RNAs, micro-RNAs, small interfering RNAs, and medium/large ncRNAs that do not belong to the aforementioned RNAs (1Mattick J.S. Makunin I.V. Hum. Mol. Genet. 2006; 15: R17-R29Crossref PubMed Scopus (1853) Google Scholar, 3Mattick J.S. Makunin I.V. Hum. Mol. Genet. 2005; 14: R121-R132Crossref PubMed Scopus (414) Google Scholar). Small nuclear RNAs and small nucleolar RNAs are usually 60–300 nucleotides long and are mainly involved in ribosome biogenesis and RNA splicing (4Matera A.G. Terns R.M. Terns M.P. Nat. Rev. Mol. PubMed Scopus Google Scholar). and small interfering RNAs are nucleotides long and function to regulate gene expression at the level J.S. Makunin I.V. Hum. Mol. Genet. 2005; 14: R121-R132Crossref PubMed Scopus (414) Google Scholar). The medium/large ncRNAs are usually in and may are that they do not encode any ncRNAs in this are they to functions K.C. Frith M.C. Mattick J.S. Trends Genet. 2006; 22: 1-5Abstract Full Text Full Text PDF PubMed Scopus (506) Google and in a of cellular to growth of and is to be tumor suppressor PubMed Scopus Google Scholar). The of cell has to inhibit growth of cells Google Scholar). The RNA functions as a in regulating transcription by nuclear Full Text Full Text PDF PubMed Scopus Google Scholar). the cellular functions of many medium/large ncRNAs non-coding RNA growth differentiation factor 15 open reading maternally expressed gene ribosomal RNA fluorescent protein isopeptide mouse double minute 2 homolog maternally expressed gene is RNA with a of nucleotides PubMed Scopus Google Scholar). mouse is PubMed Scopus Google Scholar). is a gene and is not cellular In is evidence suggesting that is to any gene with the imprinted gene the imprinted and mouse PubMed Scopus Google Scholar, Full Text Full Text PDF PubMed Scopus Google Scholar). The of this gene is by Nat. Genet. PubMed Scopus Google Scholar). that the gene of PubMed Scopus Google Scholar). to splicing PubMed Scopus Google Scholar, M.C. 14: PubMed Scopus Google Scholar). MEG3 gene transcripts of small open reading frames are found in In the proteins encoded by do not any known functional proteins Therefore, has suggested that is PubMed Scopus Google Scholar, PubMed Scopus Google Scholar). the function of MEG3 has a functional not to its MEG3 is expressed in many with the expression found in the and PubMed Scopus Google Scholar). In the is to cells PubMed Scopus Google Scholar). we found that of a cell do not MEG3 PubMed Scopus Google Scholar). In MEG3 is not expressed in many cell PubMed Scopus Google Scholar, 2005; PubMed Scopus Google Scholar). The of MEG3 expression in has found to at least in the of in the MEG3 gene as well as the 2005; PubMed Scopus Google Scholar, 2005; PubMed Scopus Google Scholar). we found that expression of MEG3 growth of cell in PubMed Scopus Google Scholar). These studies suggest that the MEG3 gene may play a role in tumor suppression. suppression is a cellular the of and the tumor suppressor p53 plays a central role in tumor suppression PubMed Scopus Google Scholar). a transcription p53 functions by regulating expression of its PubMed Scopus Google Scholar, 2005; PubMed Scopus Google Scholar). p53 is by many as and 2005; PubMed Scopus Google Scholar). activation to cell the of the and the cellular Nat. Rev. PubMed Scopus Google Scholar). p53 tumor through to cell as of tumor 2006; PubMed Scopus Google Scholar). Therefore, functional of p53 has found in PubMed Scopus Google Scholar). The of p53 is a in the p53 that p53 with and in whose the function of as that to and from p53 PubMed Scopus Google Scholar). p53 plays a critical role in tumor suppression functions of other tumor as Genet. PubMed Scopus Google PubMed Scopus Google Full Text Full Text PDF PubMed Scopus Google Trends Full Text Full Text PDF PubMed Scopus Google and J.S. Mol. 2006; 22: Full Text Full Text PDF PubMed Scopus Google Scholar). Therefore, we hypothesized that p53 may MEG3 We found that expression of MEG3 p53 and stimulates its transcription activation Using this as the functional assay, we that MEG3 functions as a non-coding RNA. In we that MEG3 stimulates expression of GDF15 through activation of p53. Finally, we that MEG3 is able to inhibit cell proliferation in the absence of p53. Our data suggest that MEG3 has a tumor suppression function, is mediated by both p53-dependent and p53-independent pathways. and its and were into the expression the of the promoter. The constructs were as and of from the of MEG3 in to of MEG3 were from MEG3 and into to and MEG3 expression constructs that a as well as a in were a with as the as Full Text Full Text PDF PubMed Scopus Google Scholar). and were in and and were in were in and in MEG3 to and to The from by to The p53-responsive from The from is expression expression of fluorescent protein the of gene promoter. MEG3 into this the of a to for and were of the GDF15 gene from to by a as from and into to of and the p53 binding from to the p53 binding in the GDF15 nucleotides and in by the as Full Text Full Text PDF PubMed Scopus Google Scholar). The GDF15 constructs were by and and cell were from the and to the and cells were by and in with were transfected with as Full Text Full Text PDF PubMed Scopus Google Scholar). p53 cells in were transfected with of of and as GDF15 cells were transfected with of constructs and of of as with cells were and were as Full Text Full Text PDF PubMed Scopus Google Scholar). 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We of from a as PubMed Scopus Google Scholar). that of the as the MEG3 by PubMed Scopus Google Scholar). from and we PubMed Scopus Google with MEG3. The of the are MEG3 as and p53 has to functions of many tumor as Genet. PubMed Scopus Google PubMed Scopus Google Trends Full Text Full Text PDF PubMed Scopus Google and J.S. Mol. 2006; 22: Full Text Full Text PDF PubMed Scopus Google Scholar). We hypothesized that p53 may play a role in the function of MEG3. this we transfected expression constructs for MEG3 and its isoforms a cell p53 and does not MEG3 We found that cells transfected with MEG3 any of its isoforms significant in p53 protein levels the p53 in cells is we used a p53-responsive to p53 with expression constructs of MEG3 and its isoforms into p53 binding at its the and has used in p53 in were in cells transfected with any of the MEG3 expression constructs in cells transfected with the that transcription from by MEG3 and its isoforms is cell we p53 in the cell functional p53 in transfection of MEG3 and its isoforms stimulates expression from These data that the p53 protein by transfection of MEG3 and its isoforms is that the activation of expression from by MEG3 and its isoforms is we in are to cells and do not functional p53. a we of with of a p53 expression and found that the of expression with that in cells transfected with In MEG3 and its isoforms to stimulate any expression at transfection in cells that of expression from by MEG3 and its isoforms is p53 MEG3 MEG3 and its isoforms we expression into cells by that p53 activation be the of a cellular to the of as MEG3 and its this we transfected cells with by of the from in cells transfected with by transfection of this to p53 accumulation in cells with this transfection of not stimulate expression from in cells These data that transfection of MEG3 does not p53 activation. transcription of MEG3 is required for p53 activation. p53 is a that its activation be by the level of cellular MEG3 transcripts in the transfected to p53 We that p53 activation is a to levels of MEG3 expression of MEG3 with a small at levels be able to a to p53 activation. p53 activation by transfection of MEG3 constructs is a MEG3 small in MEG3 may its to of the by MEG3 p53. this we a of from the of MEG3 and We transfected expression constructs into We found that MEG3 and and to any significant increase in p53 of the that expression of both to that of as demonstrated by to stimulate expression from in the MEG3 and that this is not to we in We found that expression of MEG3 and induced p53 expression of and to do In MEG3 and expression from the p53 in not These data that p53 activation by MEG3 and is a MEG3 and is not to accumulation of RNA p53 MEG3 MEG3 transcripts encode small open reading of encode with in MEG3. 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MEG3 MDM2 degradation is mainly mediated by MDM2 PubMed Scopus Google Scholar). p53 accumulation is to of we MDM2 protein levels in cells transfection with MEG3 expression we found that the MDM2 protein level in cells transfected with the with that in cells transfected with In the MDM2 level in cells transfected with expression constructs for MEG3 that in cells transfected with the with the MDM2 level in cells transfected with with that in cells transfected with with These data suggest that MEG3 and expression of We that the MDM2 protein level is in further MEG3 MDM2 expression, we MDM2 expression by cells with the with for MDM2 levels in cells of not MDM2 by MDM2 by significant in cells transfected with MEG3 and constructs with that in cells transfected with as well as in cells transfected with and These data that MEG3 MDM2 p53 by MEG3 is a transcription factor whose activation to expression of its MEG3 activation of p53 results in expression of p53 we protein levels of p21CIP1 and GDF15 in cells transfection of a MEG3 expression p21CIP1 and GDF15 are known of p53 Full Text PDF PubMed Scopus Google Scholar, PubMed Scopus Google Scholar, PubMed Scopus Google Scholar). GDF15 in a with a of and a protein Mol. PubMed Scopus Google Scholar). We GDF15 expression by levels of its in cells transfected with a expression to a significant increase in protein levels of both p21CIP1 and transfection of the MEG3 GDF15 not p21CIP1 expression, the p53 level in the cells with that in cells These results suggest that GDF15 is a gene of MEG3, p21CIP1 is the expression of GDF15 in the cells results from the p53 we transfected a MEG3 into p53 cells and that GDF15 protein in the transfected increase in GDF15 level in cells transfected with a p53 expression suggesting that MEG3 of GDF15 expression the of functional p53. These data that p53 by MEG3 is functional and is able to stimulate expression of the MEG3 stimulates GDF15 expression by transcription of the GDF15 we a a GDF15 gene of nucleotides from through and this into to a GDF15 gene as We this with expression constructs for MEG3, into We found that both and MEG3 expression from to do In we found that with into cells and MEG3 to transcription from p53 expression from in cells These data that MEG3 stimulates transcription from the GDF15 gene and this the of functional with the that MEG3 GDF15 protein levels in cells functional not in cells p53 and MEG3 GDF15 by p53 to the GDF15 GDF15 gene p53 binding PubMed Scopus Google Scholar, PubMed Scopus Google Scholar, PubMed Scopus Google Scholar). nucleotides from to from the transcription as the p53 binding the other nucleotides from through as the p53 binding We hypothesized that MEG3 stimulates GDF15 expression by to its in the GDF15 gene transcriptional expression of the this we p53 binding are required for MEG3 to transcription from the promoter. 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The p21CIP1 gene of p53 binding and p53 PubMed Scopus Google Scholar). Using we found that transfection of p53 binding to both p53 in the p21CIP1 and transfection of a MEG3 expression to increase p53 binding to in the p21CIP1 and These data that p53 by MEG3 does not stimulate transcription of the p21CIP1 that p21CIP1 is not a gene of MEG3. MEG3 in the of activation has to growth in cells Google Scholar). We MEG3 growth in We MEG3 into the expression expression of fluorescent protein The as is in cells MEG3 are by expression of a is known to p53 by MDM2 function, to growth PubMed Scopus Google Scholar). Therefore, we as a We transfected constructs into proliferation by of in cells expression of dramatically in cells with expression of We that in cells MEG3 that in cells that MEG3 proliferation in tumor cells as does its PubMed Scopus Google Scholar). the that growth suppression by transfection of to of the from to not MEG3. We found that transfection of this does not inhibit in cells the that MEG3 induced growth suppression is a cellular to the transfection of These results that transcriptional expression of MEG3 is for MEG3 of cell growth suppression by MEG3 is mediated by we in cells transfection with and is cell of in the p53 gene is by PubMed Scopus Google Scholar). of p53 expression in cells by expression of does not inhibit in cells MEG3 expression results in a significant in in the p53 is to that in cells transfected with the MEG3 indicates that MEG3 cell proliferation in the absence of p53. MEG3 as a gene is known to transcripts by splicing PubMed Scopus Google Scholar, M.C. 14: PubMed Scopus Google Scholar). We MEG3 from a PubMed Scopus Google Scholar). 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MEG3 p53 and expression of GDF15 and we that MEG3 inhibit proliferation in we found that MEG3 in cells MEG3 proliferation in cells that MEG3 can inhibit proliferation p53 and is important to that the data MEG3 of cell proliferation in the absence of p53 is not in any that p53 is not involved in MEG3 of cell proliferation in the of functional p53. has demonstrated that GDF15 proliferation of cells Mol. PubMed Scopus Google Scholar, J.S. PubMed Scopus Google is that GDF15 mediates MEG3 of cell proliferation in the of p53. These data suggest that MEG3 can inhibit cell proliferation through are p53-dependent and The is mediated by GDF15 and the is is not that many are and can tumor growth through pathways. for and for is well known to p53 by of MDM2 function Genet. PubMed Scopus Google Scholar). can cell as well as in the absence of p53 in cells 2005; Full Text Full Text PDF PubMed Scopus Google Scholar, PubMed Scopus Google Scholar). and to regulate transcription of p53 PubMed Scopus Google Scholar, A.G. Full Text Full Text PDF PubMed Scopus Google Scholar). to cell growth in the absence of p53 PubMed Scopus Google Scholar, PubMed Scopus Google Scholar, PubMed Google Scholar).

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The record

Venue

Journal of Biological Chemistry

Topic

RNA modifications and cancer

Field

Biochemistry, Genetics and Molecular Biology

Canadian institutions

—

Funders

National Institute of Diabetes and Digestive and Kidney DiseasesNational Institute on AgingNational Institutes of HealthJarislowsky Foundation

Keywords

MEG3BiologyRNALong non-coding RNATranscription (linguistics)Gene expressionMdm2Cancer researchGeneMolecular biologyGenetics

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yes

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