Tuning protein synthesis for cancer therapy

~50% of colorectal cancers have an activating mutation in KRAS (encoding the KRAS proto-oncogene) and remain difficult to target in the clinic. We have recently shown that activation of KRAS protein alters the regulation of mRNA translation, increasing total protein synthesis, and maintaining elevat...

Descripción completa

Detalles Bibliográficos
Autores principales: Knight, John R. P., Sansom, Owen J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2021
Materias:
Author’s Views
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8018481/
https://www.ncbi.nlm.nih.gov/pubmed/33855169
http://dx.doi.org/10.1080/23723556.2021.1884034
_version_ 1783674211804381184
author Knight, John R. P.
Sansom, Owen J.
author_facet Knight, John R. P.
Sansom, Owen J.
author_sort Knight, John R. P.
collection PubMed
description ~50% of colorectal cancers have an activating mutation in KRAS (encoding the KRAS proto-oncogene) and remain difficult to target in the clinic. We have recently shown that activation of KRAS protein alters the regulation of mRNA translation, increasing total protein synthesis, and maintaining elevated c-MYC (MYC proto-oncogene) expression. Targeting these pathways downstream of KRAS reveals a striking dependency that has potential for clinical translation.
format Online
Article
Text
id pubmed-8018481
institution National Center for Biotechnology Information
language English
publishDate 2021
publisher Taylor & Francis
record_format MEDLINE/PubMed
spelling pubmed-80184812021-04-13 Tuning protein synthesis for cancer therapy Knight, John R. P. Sansom, Owen J. Mol Cell Oncol Author’s Views ~50% of colorectal cancers have an activating mutation in KRAS (encoding the KRAS proto-oncogene) and remain difficult to target in the clinic. We have recently shown that activation of KRAS protein alters the regulation of mRNA translation, increasing total protein synthesis, and maintaining elevated c-MYC (MYC proto-oncogene) expression. Targeting these pathways downstream of KRAS reveals a striking dependency that has potential for clinical translation. Taylor & Francis 2021-02-22 /pmc/articles/PMC8018481/ /pubmed/33855169 http://dx.doi.org/10.1080/23723556.2021.1884034 Text en © 2021 The Author(s). Published with license by Taylor & Francis Group, LLC. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Author’s Views
Knight, John R. P.
Sansom, Owen J.
Tuning protein synthesis for cancer therapy
title Tuning protein synthesis for cancer therapy
title_full Tuning protein synthesis for cancer therapy
title_fullStr Tuning protein synthesis for cancer therapy
title_full_unstemmed Tuning protein synthesis for cancer therapy
title_short Tuning protein synthesis for cancer therapy
title_sort tuning protein synthesis for cancer therapy
topic Author’s Views
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8018481/
https://www.ncbi.nlm.nih.gov/pubmed/33855169
http://dx.doi.org/10.1080/23723556.2021.1884034
work_keys_str_mv AT knightjohnrp tuningproteinsynthesisforcancertherapy
AT sansomowenj tuningproteinsynthesisforcancertherapy

Ejemplares similares