The lncRNA MIR31HG regulates p16(INK4A) expression to modulate senescence

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Standard

The lncRNA MIR31HG regulates p16(INK4A) expression to modulate senescence. / Montes Resano, Marta; Nielsen, Morten M; Maglieri, Giulia; Jacobsen, Anders; Højfeldt, Jonas; Agrawal-Singh, Shuchi; Hansen, Klaus; Helin, Kristian; van de Werken, Harmen J G; Pedersen, Jakob S; Lund, Anders H.

In: Nature Communications, Vol. 6, 2015, p. 6967.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Montes Resano, M, Nielsen, MM, Maglieri, G, Jacobsen, A, Højfeldt, J, Agrawal-Singh, S, Hansen, K, Helin, K, van de Werken, HJG, Pedersen, JS & Lund, AH 2015, 'The lncRNA MIR31HG regulates p16(INK4A) expression to modulate senescence', Nature Communications, vol. 6, pp. 6967. https://doi.org/10.1038/ncomms7967

APA

Montes Resano, M., Nielsen, M. M., Maglieri, G., Jacobsen, A., Højfeldt, J., Agrawal-Singh, S., Hansen, K., Helin, K., van de Werken, H. J. G., Pedersen, J. S., & Lund, A. H. (2015). The lncRNA MIR31HG regulates p16(INK4A) expression to modulate senescence. Nature Communications, 6, 6967. https://doi.org/10.1038/ncomms7967

Vancouver

Montes Resano M, Nielsen MM, Maglieri G, Jacobsen A, Højfeldt J, Agrawal-Singh S et al. The lncRNA MIR31HG regulates p16(INK4A) expression to modulate senescence. Nature Communications. 2015;6:6967. https://doi.org/10.1038/ncomms7967

Author

Montes Resano, Marta ; Nielsen, Morten M ; Maglieri, Giulia ; Jacobsen, Anders ; Højfeldt, Jonas ; Agrawal-Singh, Shuchi ; Hansen, Klaus ; Helin, Kristian ; van de Werken, Harmen J G ; Pedersen, Jakob S ; Lund, Anders H. / The lncRNA MIR31HG regulates p16(INK4A) expression to modulate senescence. In: Nature Communications. 2015 ; Vol. 6. pp. 6967.

Bibtex

@article{0de091f63f954c02ad6c9b40aa98919b,
title = "The lncRNA MIR31HG regulates p16(INK4A) expression to modulate senescence",
abstract = "Oncogene-induced senescence (OIS) can occur in response to oncogenic insults and is considered an important tumour suppressor mechanism. Here we identify the lncRNA MIR31HG as upregulated in OIS and find that knockdown of MIR31HG promotes a strong p16(INK4A)-dependent senescence phenotype. Under normal conditions, MIR31HG is found in both nucleus and cytoplasm, but following B-RAF expression MIR31HG is located mainly in the cytoplasm. We show that MIR31HG interacts with both INK4A and MIR31HG genomic regions and with Polycomb group (PcG) proteins, and that MIR31HG is required for PcG-mediated repression of the INK4A locus. We further identify a functional enhancer, located between MIR31HG and INK4A, which becomes activated during OIS and interacts with the MIR31HG promoter. Data from melanoma patients show a negative correlation between MIR31HG and p16(INK4A) expression levels, suggesting a role for this transcript in cancer. Hence, our data provide a new lncRNA-mediated regulatory mechanism for the tumour suppressor p16(INK4A).",
author = "{Montes Resano}, Marta and Nielsen, {Morten M} and Giulia Maglieri and Anders Jacobsen and Jonas H{\o}jfeldt and Shuchi Agrawal-Singh and Klaus Hansen and Kristian Helin and {van de Werken}, {Harmen J G} and Pedersen, {Jakob S} and Lund, {Anders H.}",
year = "2015",
doi = "10.1038/ncomms7967",
language = "English",
volume = "6",
pages = "6967",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "nature publishing group",

}

RIS

TY - JOUR

T1 - The lncRNA MIR31HG regulates p16(INK4A) expression to modulate senescence

AU - Montes Resano, Marta

AU - Nielsen, Morten M

AU - Maglieri, Giulia

AU - Jacobsen, Anders

AU - Højfeldt, Jonas

AU - Agrawal-Singh, Shuchi

AU - Hansen, Klaus

AU - Helin, Kristian

AU - van de Werken, Harmen J G

AU - Pedersen, Jakob S

AU - Lund, Anders H.

PY - 2015

Y1 - 2015

N2 - Oncogene-induced senescence (OIS) can occur in response to oncogenic insults and is considered an important tumour suppressor mechanism. Here we identify the lncRNA MIR31HG as upregulated in OIS and find that knockdown of MIR31HG promotes a strong p16(INK4A)-dependent senescence phenotype. Under normal conditions, MIR31HG is found in both nucleus and cytoplasm, but following B-RAF expression MIR31HG is located mainly in the cytoplasm. We show that MIR31HG interacts with both INK4A and MIR31HG genomic regions and with Polycomb group (PcG) proteins, and that MIR31HG is required for PcG-mediated repression of the INK4A locus. We further identify a functional enhancer, located between MIR31HG and INK4A, which becomes activated during OIS and interacts with the MIR31HG promoter. Data from melanoma patients show a negative correlation between MIR31HG and p16(INK4A) expression levels, suggesting a role for this transcript in cancer. Hence, our data provide a new lncRNA-mediated regulatory mechanism for the tumour suppressor p16(INK4A).

AB - Oncogene-induced senescence (OIS) can occur in response to oncogenic insults and is considered an important tumour suppressor mechanism. Here we identify the lncRNA MIR31HG as upregulated in OIS and find that knockdown of MIR31HG promotes a strong p16(INK4A)-dependent senescence phenotype. Under normal conditions, MIR31HG is found in both nucleus and cytoplasm, but following B-RAF expression MIR31HG is located mainly in the cytoplasm. We show that MIR31HG interacts with both INK4A and MIR31HG genomic regions and with Polycomb group (PcG) proteins, and that MIR31HG is required for PcG-mediated repression of the INK4A locus. We further identify a functional enhancer, located between MIR31HG and INK4A, which becomes activated during OIS and interacts with the MIR31HG promoter. Data from melanoma patients show a negative correlation between MIR31HG and p16(INK4A) expression levels, suggesting a role for this transcript in cancer. Hence, our data provide a new lncRNA-mediated regulatory mechanism for the tumour suppressor p16(INK4A).

U2 - 10.1038/ncomms7967

DO - 10.1038/ncomms7967

M3 - Journal article

C2 - 25908244

VL - 6

SP - 6967

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

ER -

ID: 136668732