Cited by 1,115Pluripotent Stem Cells ResearchDevelopmental Biology and Gene RegulationCancer-related Molecular Pathways

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Linking the p53 tumour suppressor pathway to somatic cell reprogramming

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Kawamura, Teruhisa, Suzuki, Jotaro, Wang, Yunyuan V., Menendez, Sergio, Morera, Laura Batlle, Raya, Angel, Wahl, Geoffrey M., Belmonte, Juan Carlos Izpisúa·2009·Nature

DOI 10.1038/nature08311PMC PMC2735889

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Abstract

Reprogramming somatic cells to induced pluripotent stem (iPS) cells has been accomplished by expressing pluripotency factors and oncogenes, but the low frequency and tendency to induce malignant transformation compromise the clinical utility of this powerful approach. We address both issues by investigating the mechanisms limiting reprogramming efficiency in somatic cells. Here we show that reprogramming factors can activate the p53 (also known as Trp53 in mice, TP53 in humans) pathway. Reducing signalling to p53 by expressing a mutated version of one of its negative regulators, by deleting or knocking down p53 or its target gene, p21 (also known as Cdkn1a), or by antagonizing reprogramming-induced apoptosis in mouse fibroblasts increases reprogramming efficiency. Notably, decreasing p53 protein levels enabled fibroblasts to give rise to iPS cells capable of generating germline-transmitting chimaeric mice using only Oct4 (also known as Pou5f1) and Sox2. Furthermore, silencing of p53 significantly increased the reprogramming efficiency of human somatic cells. These results provide insights into reprogramming mechanisms and suggest new routes to more efficient reprogramming while minimizing the use of oncogenes.

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Authors: Kawamura, T., Suzuki, J., Wang, Y. V., Menendez, S., Morera, L. B., Raya, A., Wahl, G. M., & Belmonte, J. C. I.
Affiliations: Salk Institute for Biological Studies (US)
Corresponding author: Wahl, Geoffrey M.
Belmonte, Juan Carlos Izpisúa
ORCID: Kawamura, Teruhisa
Wahl, Geoffrey M.
Belmonte, Juan Carlos Izpisúa
Venue: Nature
Publisher: Springer Science and Business Media LLC
Published: 2009-08
Volume: 460
Issue: 7259
Pages: 1140-1144
ISSN: 0028-0836 (ISSN-L)
1476-4687
DOI: 10.1038/nature08311
PMC: PMC2735889
OpenAlex: W2070672434
Cited by: 1,115
References: 40
Citations by year: 2026: 13 · 2025: 12 · 2024: 30 · 2023: 34 · 2022: 31 · 2021: 36 · 2020: 29 · 2019: 41 · 2018: 55 · 2017: 60 · 2016: 65 · 2015: 77 · 2014: 96 · 2013: 111 · 2012: 136
FWCI: 57.10
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Nature (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
RePEc: Research Papers in Economics (submittedVersion)
Funders: National Heart, Lung, and Blood Institute (R33HL088293)
National Cancer Institute (R01CA100845, R01CA061449)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pluripotent Stem Cells Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Keywords: p53, somatic cell reprogramming, induced pluripotent stem cells, Oct4, SOX2, p21, Nutlin-3, reprogramming efficiency, malignant transformation, fibroblasts, oncogenes, apoptosis
MeSH terms: Animals, Cells, Cultured, Embryo, Mammalian, Female, Fibroblasts, Humans, Male, Mice, Inbred C57BL, Down-Regulation, Keratinocytes, Tumor Suppressor Protein p53, Pluripotent Stem Cells, Cyclin-Dependent Kinase Inhibitor p21, Mice, Cellular Reprogramming

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Linking the p53 tumour suppressor pathway to somatic cell reprogramming

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