RNA polymerase III transcription is repressed in response to the tumour suppressor ARF

Jennifer P. Morton; Theodoros Kantidakis; Robert J. White

doi:10.1093/nar/gkm208

RNA polymerase III transcription is repressed in response to the tumour suppressor ARF

Jennifer P. Morton
, Theodoros Kantidakis
, Robert J. White^*

^*Corresponding author for this work

Aston Medical School

University of Glasgow
Division of Biochemistry and Molecular Biology
Beatson Institute for Cancer Research

Research output: Contribution to journal › Article › peer-review

19 Citations (Scopus)

53 Downloads (Pure)

Abstract

The tumour suppressor protein ARF provides a defence mechanism against hyperproliferative stresses that can result from the aberrant activation of oncogenes. Accordingly, ARF is silenced or deleted in many human cancers. Activation of ARF can arrest growth and cell cycle progression, or trigger apoptosis. A principle mediator of these effects is p53, which ARF stabilizes by binding and inhibiting MDM2. However, ARF has additional targets and remains able to block growth in the absence of p53, albeit less efficiently. For example, ARF can suppress rRNA production in a p53-independent manner. We have found that the synthesis of tRNA by RNA polymerase III is also inhibited in response to ARF. However, in contrast to its effects on rRNA synthesis, ARF is unable to inhibit tRNA gene transcription when p53 is ablated. These results add to the growing list of cellular changes that can be triggered by ARF induction.

Original language	English
Pages (from-to)	3046-3052
Number of pages	7
Journal	Nucleic Acids Research
Volume	35
Issue number	9
DOIs	https://doi.org/10.1093/nar/gkm208
Publication status	Published - 1 May 2007

Bibliographical note

© 2007 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Funding

The authors are grateful to Gordon Peters for NARF2 and E6-NARF2 cell lines. This work was funded by the Wellcome Trust and Cancer Research UK. Funding to pay the Open Access publication charges for this article was provided by the Wellcome Trust.

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

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10.1093/nar/gkm208Licence: CC BY-NC 3.0

RNA polymerase III transcription is repressed in response to the tumour suppressor ARF
© 2007 The Author(s) This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Final published version, 591 KBLicence: CC BY-NC 3.0

Cite this

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title = "RNA polymerase III transcription is repressed in response to the tumour suppressor ARF",

abstract = "The tumour suppressor protein ARF provides a defence mechanism against hyperproliferative stresses that can result from the aberrant activation of oncogenes. Accordingly, ARF is silenced or deleted in many human cancers. Activation of ARF can arrest growth and cell cycle progression, or trigger apoptosis. A principle mediator of these effects is p53, which ARF stabilizes by binding and inhibiting MDM2. However, ARF has additional targets and remains able to block growth in the absence of p53, albeit less efficiently. For example, ARF can suppress rRNA production in a p53-independent manner. We have found that the synthesis of tRNA by RNA polymerase III is also inhibited in response to ARF. However, in contrast to its effects on rRNA synthesis, ARF is unable to inhibit tRNA gene transcription when p53 is ablated. These results add to the growing list of cellular changes that can be triggered by ARF induction.",

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AB - The tumour suppressor protein ARF provides a defence mechanism against hyperproliferative stresses that can result from the aberrant activation of oncogenes. Accordingly, ARF is silenced or deleted in many human cancers. Activation of ARF can arrest growth and cell cycle progression, or trigger apoptosis. A principle mediator of these effects is p53, which ARF stabilizes by binding and inhibiting MDM2. However, ARF has additional targets and remains able to block growth in the absence of p53, albeit less efficiently. For example, ARF can suppress rRNA production in a p53-independent manner. We have found that the synthesis of tRNA by RNA polymerase III is also inhibited in response to ARF. However, in contrast to its effects on rRNA synthesis, ARF is unable to inhibit tRNA gene transcription when p53 is ablated. These results add to the growing list of cellular changes that can be triggered by ARF induction.

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RNA polymerase III transcription is repressed in response to the tumour suppressor ARF

Abstract

Bibliographical note

Funding

UN SDGs

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