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Expression of oncogenic HRAS (G12V) causes defects in control of cell size in NIH 3T3 cells

Severe defects in control of cell size are closely associated with cancer. However, the mechanisms that drive cell size defects in cancer remain unknown and it is unclear whether they are a direct consequence of signals from primary oncogenic drivers or a secondary consequence of mutations that accu...

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Detalles Bibliográficos
Autores principales: DeWitt, Jerry T., Sharma, Michael V., Kellogg, Douglas R.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Caltech Library 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10654777/
https://www.ncbi.nlm.nih.gov/pubmed/38021173
http://dx.doi.org/10.17912/micropub.biology.000873
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author DeWitt, Jerry T.
Sharma, Michael V.
Kellogg, Douglas R.
author_facet DeWitt, Jerry T.
Sharma, Michael V.
Kellogg, Douglas R.
author_sort DeWitt, Jerry T.
collection PubMed
description Severe defects in control of cell size are closely associated with cancer. However, the mechanisms that drive cell size defects in cancer remain unknown and it is unclear whether they are a direct consequence of signals from primary oncogenic drivers or a secondary consequence of mutations that accumulate during evolution of cancer cells. Here, we report that expression of oncogenic HRAS (G12V) is sufficient to cause cell size defects in NIH 3T3 cells, which suggests that the cell size defects of cancer cells are a direct consequence of primary oncogenic drivers.
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spelling pubmed-106547772023-11-02 Expression of oncogenic HRAS (G12V) causes defects in control of cell size in NIH 3T3 cells DeWitt, Jerry T. Sharma, Michael V. Kellogg, Douglas R. MicroPubl Biol New Finding Severe defects in control of cell size are closely associated with cancer. However, the mechanisms that drive cell size defects in cancer remain unknown and it is unclear whether they are a direct consequence of signals from primary oncogenic drivers or a secondary consequence of mutations that accumulate during evolution of cancer cells. Here, we report that expression of oncogenic HRAS (G12V) is sufficient to cause cell size defects in NIH 3T3 cells, which suggests that the cell size defects of cancer cells are a direct consequence of primary oncogenic drivers. Caltech Library 2023-11-02 /pmc/articles/PMC10654777/ /pubmed/38021173 http://dx.doi.org/10.17912/micropub.biology.000873 Text en Copyright: © 2023 by the authors https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle New Finding
DeWitt, Jerry T.
Sharma, Michael V.
Kellogg, Douglas R.
Expression of oncogenic HRAS (G12V) causes defects in control of cell size in NIH 3T3 cells
title Expression of oncogenic HRAS (G12V) causes defects in control of cell size in NIH 3T3 cells
title_full Expression of oncogenic HRAS (G12V) causes defects in control of cell size in NIH 3T3 cells
title_fullStr Expression of oncogenic HRAS (G12V) causes defects in control of cell size in NIH 3T3 cells
title_full_unstemmed Expression of oncogenic HRAS (G12V) causes defects in control of cell size in NIH 3T3 cells
title_short Expression of oncogenic HRAS (G12V) causes defects in control of cell size in NIH 3T3 cells
title_sort expression of oncogenic hras (g12v) causes defects in control of cell size in nih 3t3 cells
topic New Finding
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10654777/
https://www.ncbi.nlm.nih.gov/pubmed/38021173
http://dx.doi.org/10.17912/micropub.biology.000873
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