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p53-independent upregulation of miR-34a during oncogene-induced senescence represses MYC

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Christoffersen, NR, Shalgi, R, Frankel, L, Leucci, E, Lees, MJ, Klausen, M, Pilpel, Y, Nielsen, FC, Oren, M & Lund, AH 2010, 'p53-independent upregulation of miR-34a during oncogene-induced senescence represses MYC', Cell Death and Differentiation, vol. 17, no. 2, pp. 236-45. https://doi.org/10.1038/cdd.2009.109

APA

Christoffersen, N. R., Shalgi, R., Frankel, L., Leucci, E., Lees, M. J., Klausen, M., Pilpel, Y., Nielsen, F. C., Oren, M., & Lund, A. H. (2010). p53-independent upregulation of miR-34a during oncogene-induced senescence represses MYC. Cell Death and Differentiation, 17(2), 236-45. https://doi.org/10.1038/cdd.2009.109

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MLA

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Author

Christoffersen, N R ; Shalgi, R ; Frankel, Lisa ; Leucci, Eleonora ; Lees, Michael James ; Klausen, Mikkel ; Pilpel, Y ; Nielsen, F C ; Oren, M ; Lund, A H. / p53-independent upregulation of miR-34a during oncogene-induced senescence represses MYC. In: Cell Death and Differentiation. 2010 ; Vol. 17, No. 2. pp. 236-45.

Bibtex

@article{fb74933537c64be0aa01de64627d7faf,
title = "p53-independent upregulation of miR-34a during oncogene-induced senescence represses MYC",
abstract = "Aberrant oncogene activation induces cellular senescence, an irreversible growth arrest that acts as a barrier against tumorigenesis. To identify microRNAs (miRNAs) involved in oncogene-induced senescence, we examined the expression of miRNAs in primary human TIG3 fibroblasts after constitutive activation of B-RAF. Among the regulated miRNAs, both miR-34a and miR-146a were strongly induced during senescence. Although members of the miR-34 family are known to be transcriptionally regulated by p53, we find that miR-34a is regulated independently of p53 during oncogene-induced senescence. Instead, upregulation of miR-34a is mediated by the ETS family transcription factor, ELK1. During senescence, miR-34a targets the important proto-oncogene MYC and our data suggest that miR-34a thereby coordinately controls a set of cell cycle regulators. Hence, in addition to its integration in the p53 pathway, we show that alternative cancer-related pathways regulate miR-34a, emphasising its significance as a tumour suppressor.",
author = "Christoffersen, {N R} and R Shalgi and Lisa Frankel and Eleonora Leucci and Lees, {Michael James} and Mikkel Klausen and Y Pilpel and Nielsen, {F C} and M Oren and Lund, {A H}",
year = "2010",
month = feb,
day = "1",
doi = "10.1038/cdd.2009.109",
language = "English",
volume = "17",
pages = "236--45",
journal = "Cell Death and Differentiation",
issn = "1350-9047",
publisher = "Nature Publishing Group",
number = "2",

}

RIS

TY - JOUR

T1 - p53-independent upregulation of miR-34a during oncogene-induced senescence represses MYC

AU - Christoffersen, N R

AU - Shalgi, R

AU - Frankel, Lisa

AU - Leucci, Eleonora

AU - Lees, Michael James

AU - Klausen, Mikkel

AU - Pilpel, Y

AU - Nielsen, F C

AU - Oren, M

AU - Lund, A H

PY - 2010/2/1

Y1 - 2010/2/1

N2 - Aberrant oncogene activation induces cellular senescence, an irreversible growth arrest that acts as a barrier against tumorigenesis. To identify microRNAs (miRNAs) involved in oncogene-induced senescence, we examined the expression of miRNAs in primary human TIG3 fibroblasts after constitutive activation of B-RAF. Among the regulated miRNAs, both miR-34a and miR-146a were strongly induced during senescence. Although members of the miR-34 family are known to be transcriptionally regulated by p53, we find that miR-34a is regulated independently of p53 during oncogene-induced senescence. Instead, upregulation of miR-34a is mediated by the ETS family transcription factor, ELK1. During senescence, miR-34a targets the important proto-oncogene MYC and our data suggest that miR-34a thereby coordinately controls a set of cell cycle regulators. Hence, in addition to its integration in the p53 pathway, we show that alternative cancer-related pathways regulate miR-34a, emphasising its significance as a tumour suppressor.

AB - Aberrant oncogene activation induces cellular senescence, an irreversible growth arrest that acts as a barrier against tumorigenesis. To identify microRNAs (miRNAs) involved in oncogene-induced senescence, we examined the expression of miRNAs in primary human TIG3 fibroblasts after constitutive activation of B-RAF. Among the regulated miRNAs, both miR-34a and miR-146a were strongly induced during senescence. Although members of the miR-34 family are known to be transcriptionally regulated by p53, we find that miR-34a is regulated independently of p53 during oncogene-induced senescence. Instead, upregulation of miR-34a is mediated by the ETS family transcription factor, ELK1. During senescence, miR-34a targets the important proto-oncogene MYC and our data suggest that miR-34a thereby coordinately controls a set of cell cycle regulators. Hence, in addition to its integration in the p53 pathway, we show that alternative cancer-related pathways regulate miR-34a, emphasising its significance as a tumour suppressor.

U2 - 10.1038/cdd.2009.109

DO - 10.1038/cdd.2009.109

M3 - Journal article

C2 - 19696787

VL - 17

SP - 236

EP - 245

JO - Cell Death and Differentiation

JF - Cell Death and Differentiation

SN - 1350-9047

IS - 2

ER -

ID: 31046382