The long non-coding RNA MIR31HG regulates the senescence associated secretory phenotype

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The long non-coding RNA MIR31HG regulates the senescence associated secretory phenotype. / Montes, Marta; Lubas, Michal; Arendrup, Frederic S; Mentz, Bettina; Rohatgi, Neha; Tumas, Sarunas; Harder, Lea M; Skanderup, Anders J; Andersen, Jens S; Lund, Anders H.

In: Nature Communications, Vol. 12, No. 1, 2459, 2021, p. 1-17.

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

Harvard

Montes, M, Lubas, M, Arendrup, FS, Mentz, B, Rohatgi, N, Tumas, S, Harder, LM, Skanderup, AJ, Andersen, JS & Lund, AH 2021, 'The long non-coding RNA MIR31HG regulates the senescence associated secretory phenotype', Nature Communications, vol. 12, no. 1, 2459, pp. 1-17. https://doi.org/10.1038/s41467-021-22746-4

APA

Montes, M., Lubas, M., Arendrup, F. S., Mentz, B., Rohatgi, N., Tumas, S., Harder, L. M., Skanderup, A. J., Andersen, J. S., & Lund, A. H. (2021). The long non-coding RNA MIR31HG regulates the senescence associated secretory phenotype. Nature Communications, 12(1), 1-17. [2459]. https://doi.org/10.1038/s41467-021-22746-4

Vancouver

Montes M, Lubas M, Arendrup FS, Mentz B, Rohatgi N, Tumas S et al. The long non-coding RNA MIR31HG regulates the senescence associated secretory phenotype. Nature Communications. 2021;12(1):1-17. 2459. https://doi.org/10.1038/s41467-021-22746-4

Author

Montes, Marta ; Lubas, Michal ; Arendrup, Frederic S ; Mentz, Bettina ; Rohatgi, Neha ; Tumas, Sarunas ; Harder, Lea M ; Skanderup, Anders J ; Andersen, Jens S ; Lund, Anders H. / The long non-coding RNA MIR31HG regulates the senescence associated secretory phenotype. In: Nature Communications. 2021 ; Vol. 12, No. 1. pp. 1-17.

Bibtex

@article{0a1643e6dc8046adb1fb416ec3e624a3,
title = "The long non-coding RNA MIR31HG regulates the senescence associated secretory phenotype",
abstract = "Oncogene-induced senescence provides a barrier against malignant transformation. However, it can also promote cancer through the secretion of a plethora of factors released by senescent cells, called the senescence associated secretory phenotype (SASP). We have previously shown that in proliferating cells, nuclear lncRNA MIR31HG inhibits p16/CDKN2A expression through interaction with polycomb repressor complexes and that during BRAF-induced senescence, MIR31HG is overexpressed and translocates to the cytoplasm. Here, we show that MIR31HG regulates the expression and secretion of a subset of SASP components during BRAF-induced senescence. The SASP secreted from senescent cells depleted for MIR31HG fails to induce paracrine invasion without affecting the growth inhibitory effect. Mechanistically, MIR31HG interacts with YBX1 facilitating its phosphorylation at serine 102 (p-YBX1S102) by the kinase RSK. p-YBX1S102 induces IL1A translation which activates the transcription of the other SASP mRNAs. Our results suggest a dual role for MIR31HG in senescence depending on its localization and points to the lncRNA as a potential therapeutic target in the treatment of senescence-related pathologies.",
author = "Marta Montes and Michal Lubas and Arendrup, {Frederic S} and Bettina Mentz and Neha Rohatgi and Sarunas Tumas and Harder, {Lea M} and Skanderup, {Anders J} and Andersen, {Jens S} and Lund, {Anders H}",
year = "2021",
doi = "10.1038/s41467-021-22746-4",
language = "English",
volume = "12",
pages = "1--17",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "nature publishing group",
number = "1",

}

RIS

TY - JOUR

T1 - The long non-coding RNA MIR31HG regulates the senescence associated secretory phenotype

AU - Montes, Marta

AU - Lubas, Michal

AU - Arendrup, Frederic S

AU - Mentz, Bettina

AU - Rohatgi, Neha

AU - Tumas, Sarunas

AU - Harder, Lea M

AU - Skanderup, Anders J

AU - Andersen, Jens S

AU - Lund, Anders H

PY - 2021

Y1 - 2021

N2 - Oncogene-induced senescence provides a barrier against malignant transformation. However, it can also promote cancer through the secretion of a plethora of factors released by senescent cells, called the senescence associated secretory phenotype (SASP). We have previously shown that in proliferating cells, nuclear lncRNA MIR31HG inhibits p16/CDKN2A expression through interaction with polycomb repressor complexes and that during BRAF-induced senescence, MIR31HG is overexpressed and translocates to the cytoplasm. Here, we show that MIR31HG regulates the expression and secretion of a subset of SASP components during BRAF-induced senescence. The SASP secreted from senescent cells depleted for MIR31HG fails to induce paracrine invasion without affecting the growth inhibitory effect. Mechanistically, MIR31HG interacts with YBX1 facilitating its phosphorylation at serine 102 (p-YBX1S102) by the kinase RSK. p-YBX1S102 induces IL1A translation which activates the transcription of the other SASP mRNAs. Our results suggest a dual role for MIR31HG in senescence depending on its localization and points to the lncRNA as a potential therapeutic target in the treatment of senescence-related pathologies.

AB - Oncogene-induced senescence provides a barrier against malignant transformation. However, it can also promote cancer through the secretion of a plethora of factors released by senescent cells, called the senescence associated secretory phenotype (SASP). We have previously shown that in proliferating cells, nuclear lncRNA MIR31HG inhibits p16/CDKN2A expression through interaction with polycomb repressor complexes and that during BRAF-induced senescence, MIR31HG is overexpressed and translocates to the cytoplasm. Here, we show that MIR31HG regulates the expression and secretion of a subset of SASP components during BRAF-induced senescence. The SASP secreted from senescent cells depleted for MIR31HG fails to induce paracrine invasion without affecting the growth inhibitory effect. Mechanistically, MIR31HG interacts with YBX1 facilitating its phosphorylation at serine 102 (p-YBX1S102) by the kinase RSK. p-YBX1S102 induces IL1A translation which activates the transcription of the other SASP mRNAs. Our results suggest a dual role for MIR31HG in senescence depending on its localization and points to the lncRNA as a potential therapeutic target in the treatment of senescence-related pathologies.

U2 - 10.1038/s41467-021-22746-4

DO - 10.1038/s41467-021-22746-4

M3 - Journal article

C2 - 33911076

VL - 12

SP - 1

EP - 17

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

IS - 1

M1 - 2459

ER -

ID: 260879952