Piunti, A., Rossi, A., Cerutti, A., Albert, M., Jammula, S., Scelfo, A., Cedrone, L., Fragola, G., Pålsson, L. E., Koseki, H., Testa, G., Casola, S., Helin, K., d'Adda di Fagagna, F., & Pasini, D. (2014). Polycomb proteins control proliferation and transformation independently of cell cycle checkpoints by regulating DNA replication. Nature Communications, 5, 3649. https://doi.org/10.1038/ncomms4649
Polycomb proteins control proliferation and transformation independently of cell cycle checkpoints by regulating DNA replication. / Piunti, Andrea; Rossi, Alessandra; Cerutti, Aurora et al.
In:
Nature Communications, Vol. 5, 14.04.2014, p. 3649.
Research output: Contribution to journal › Journal article › Research › peer-review
Piunti, A, Rossi, A, Cerutti, A, Albert, M, Jammula, S, Scelfo, A, Cedrone, L, Fragola, G, Pålsson, LE, Koseki, H, Testa, G, Casola, S, Helin, K, d'Adda di Fagagna, F & Pasini, D 2014, 'Polycomb proteins control proliferation and transformation independently of cell cycle checkpoints by regulating DNA replication', Nature Communications, vol. 5, pp. 3649. https://doi.org/10.1038/ncomms4649
Piunti A, Rossi A, Cerutti A, Albert M, Jammula S, Scelfo A et al. Polycomb proteins control proliferation and transformation independently of cell cycle checkpoints by regulating DNA replication. Nature Communications. 2014 Apr 14;5:3649. doi: 10.1038/ncomms4649
Piunti, Andrea ; Rossi, Alessandra ; Cerutti, Aurora et al. / Polycomb proteins control proliferation and transformation independently of cell cycle checkpoints by regulating DNA replication. In: Nature Communications. 2014 ; Vol. 5. pp. 3649.
@article{6275be378759479392cd84cfc28cacd4,
title = "Polycomb proteins control proliferation and transformation independently of cell cycle checkpoints by regulating DNA replication",
abstract = "The ability of PRC1 and PRC2 to promote proliferation is a main feature that links polycomb (PcG) activity to cancer. PcGs silence the expression of the tumour suppressor locus Ink4a/Arf, whose products positively regulate pRb and p53 functions. Enhanced PcG activity is a frequent feature of human tumours, and PcG inhibition has been proposed as a strategy for cancer treatment. However, the recurrent inactivation of pRb/p53 responses in human cancers raises a question regarding the ability of PcG proteins to affect cellular proliferation independently from this checkpoint. Here we demonstrate that PRCs regulate cellular proliferation and transformation independently of the Ink4a/Arf-pRb-p53 pathway. We provide evidence that PRCs localize at replication forks, and that loss of their function directly affects the progression and symmetry of DNA replication forks. Thus, we have identified a novel activity by which PcGs can regulate cell proliferation independently of major cell cycle restriction checkpoints.",
author = "Andrea Piunti and Alessandra Rossi and Aurora Cerutti and Mareike Albert and Sriganesh Jammula and Andrea Scelfo and Laura Cedrone and Giulia Fragola and P{\aa}lsson, {Linda Elin} and Haruhiko Koseki and Giuseppe Testa and Stefano Casola and Kristian Helin and {d'Adda di Fagagna}, Fabrizio and Diego Pasini",
year = "2014",
month = apr,
day = "14",
doi = "10.1038/ncomms4649",
language = "English",
volume = "5",
pages = "3649",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "nature publishing group",
}
TY - JOUR
T1 - Polycomb proteins control proliferation and transformation independently of cell cycle checkpoints by regulating DNA replication
AU - Piunti, Andrea
AU - Rossi, Alessandra
AU - Cerutti, Aurora
AU - Albert, Mareike
AU - Jammula, Sriganesh
AU - Scelfo, Andrea
AU - Cedrone, Laura
AU - Fragola, Giulia
AU - Pålsson, Linda Elin
AU - Koseki, Haruhiko
AU - Testa, Giuseppe
AU - Casola, Stefano
AU - Helin, Kristian
AU - d'Adda di Fagagna, Fabrizio
AU - Pasini, Diego
PY - 2014/4/14
Y1 - 2014/4/14
N2 - The ability of PRC1 and PRC2 to promote proliferation is a main feature that links polycomb (PcG) activity to cancer. PcGs silence the expression of the tumour suppressor locus Ink4a/Arf, whose products positively regulate pRb and p53 functions. Enhanced PcG activity is a frequent feature of human tumours, and PcG inhibition has been proposed as a strategy for cancer treatment. However, the recurrent inactivation of pRb/p53 responses in human cancers raises a question regarding the ability of PcG proteins to affect cellular proliferation independently from this checkpoint. Here we demonstrate that PRCs regulate cellular proliferation and transformation independently of the Ink4a/Arf-pRb-p53 pathway. We provide evidence that PRCs localize at replication forks, and that loss of their function directly affects the progression and symmetry of DNA replication forks. Thus, we have identified a novel activity by which PcGs can regulate cell proliferation independently of major cell cycle restriction checkpoints.
AB - The ability of PRC1 and PRC2 to promote proliferation is a main feature that links polycomb (PcG) activity to cancer. PcGs silence the expression of the tumour suppressor locus Ink4a/Arf, whose products positively regulate pRb and p53 functions. Enhanced PcG activity is a frequent feature of human tumours, and PcG inhibition has been proposed as a strategy for cancer treatment. However, the recurrent inactivation of pRb/p53 responses in human cancers raises a question regarding the ability of PcG proteins to affect cellular proliferation independently from this checkpoint. Here we demonstrate that PRCs regulate cellular proliferation and transformation independently of the Ink4a/Arf-pRb-p53 pathway. We provide evidence that PRCs localize at replication forks, and that loss of their function directly affects the progression and symmetry of DNA replication forks. Thus, we have identified a novel activity by which PcGs can regulate cell proliferation independently of major cell cycle restriction checkpoints.
U2 - 10.1038/ncomms4649
DO - 10.1038/ncomms4649
M3 - Journal article
C2 - 24728135
SN - 2041-1723
VL - 5
SP - 3649
JO - Nature Communications
JF - Nature Communications
ER -
