The DOI matches its Crossref record; 63 of the 63 references it cites were found in a registry or an index.
New plays in the p53 theater
Open accessAbstract
The p53 tumor suppressor and its paralogs p63 and p73 are at the crux of a network modulating cellular responses against potentially tumorigenic events. p53 acts primarily as a transcription factor, regulating the expression of both coding and non-coding RNAs, as well as the activity of RNA processing complexes. In line with their anti-tumorigenic function, p53 and p63 have recently been implicated in restricting tumor cell invasion. In parallel, a growing number of non-canonical target genes have been added to the p53 repertoire. These include genes encoding for proteins that impinge on a broad spectrum of cellular functions, from cell metabolism to stem cell renewal. The p53 story is still far from being fully told.
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“For instance, a missense mutation in the p53 transcription factor, which can be held accountable for tumor initiation, development, and growth in more than half of solid tumor cancers [32].”
From Microfluidic modelling of the tumor microenvironment for anti-cancer drug development (2019) · cites this paper as [32]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Briefly, the p53 protein acts as a tumor suppressor as it induces apoptosis when cellular mutations occur and initiate DNA repairs in healthy cells [32].”
From Microfluidic modelling of the tumor microenvironment for anti-cancer drug development (2019) · cites this paper as [32]
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Citations
Cites
Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Donehower, L. A., Harvey, M., Slagle, B. L., McArthur, M. J., Montgomery, C. A., Butel, J. S., & Bradley, A. (1992) · Nature · doi:10.1038/356215a0 · Cited by 4,649 · cited 1×
“p53 knockout mice develop tumors with short latency and 100% penetrance [3].”
BackgroundChromatin signature reveals over a thousand highly conserved large non-coding RNAs in mammals
Guttman, M., Amit, I., Garber, M., French, C., Lin, M. F., Feldser, D., Huarte, M., Zuk, O., Carey, B. W., Cassady, J. P., et al. (2009) · Nature · doi:10.1038/nature07672 · Cited by 4,098 · cited 1×
“Other classes of non-coding RNA such as large intervening non-coding RNA (lincRNA) are also regulated by p53 [24].”
BackgroundBlinded by the Light: The Growing Complexity of p53
Vousden, K. H., & Prives, C. (2009) · Cell · doi:10.1016/j.cell.2009.04.037 · Cited by 3,163 · cited 2×
“Biochemically, p53 is a potent transcriptional regulator capable of controlling the expression of hundreds of genes [4,5].”
BackgroundKhalil, A. M., Guttman, M., Huarte, M., Garber, M., Raj, A., Rivea Morales, D., Thomas, K., Presser, A., Bernstein, B. E., van Oudenaarden, A., et al. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0904715106 · Cited by 2,872 · cited 1×
“For instance, the p53-induced lincRNA TUG1 facilitates repression of cell cycle-related genes through binding the polycomb repression complex PRC2 [25].”
BackgroundA microRNA component of the p53 tumour suppressor network
He, L., He, X., Lim, L. P., de Stanchina, E., Xuan, Z., Liang, Y., Xue, W., Zender, L., Magnus, J., Ridzon, D., et al. (2007) · Nature · doi:10.1038/nature05939 · Cited by 2,692 · cited 1×
“p53 modulates the expression of numerous miRNA species, including miR34a,b and c [17,18].”
BackgroundTIGAR, a p53-Inducible Regulator of Glycolysis and Apoptosis
Bensaad, K., Tsuruta, A., Selak, M. A., Vidal, M. N. C., Nakano, K., Bartrons, R., Gottlieb, E., & Vousden, K. H. (2006) · Cell · doi:10.1016/j.cell.2006.05.036 · Cited by 2,019 · cited 1×
“p53 antagonizes the Warburg Effect and inhibits glycolysis by decreasing glucose uptake [8], inducing glycolysis-repressing genes [9] and enhancing mitochondrial respiration [10] (Figure 1a).”
BackgroundThe first 30 years of p53: growing ever more complex.
Levine, A. J., & Oren, M. (2009) · Nature Reviews Cancer · doi:10.1038/nrc2723 · Cited by 1,967 · cited 2×
“The p53 response is elicited by a wide variety of stress signals conducive to or associated with malignant transformation, such as DNA damage, oncogene activation, abnormal mitosis, loss of cell–cell contact and hypoxia [5].”
BackgroundSelf-citationAMP-activated protein kinase induces a p53-dependent metabolic checkpoint
Jones, R. G., Plas, D. R., Kubek, S., Buzzai, M., Mu, J., Xu, Y., Birnbaum, M. J., & Thompson, C. B. (2005) · Molecular Cell · doi:10.1016/j.molcel.2005.03.027 · Cited by 1,619 · cited 1×
“Perhaps not surprisingly, AMPK both activates and is activated by p53 in response to energetic stress [12,13].”
BackgroundDRAM, a p53-Induced Modulator of Autophagy, Is Critical for Apoptosis
Crighton, D., Wilkinson, S., O'Prey, J., Syed, N., Smith, P., Harrison, P. R., Gasco, M., Garrone, O., Crook, T., & Ryan, K. M. (2006) · Cell · doi:10.1016/j.cell.2006.05.034 · Cited by 1,380
Transcriptional Activation of miR-34a Contributes to p53-Mediated Apoptosis
Raver-Shapira, N., Marciano, E., Meiri, E., Spector, Y., Rosenfeld, N., Moskovits, N. B.-C., Bentwich, Z., & Oren, M. (2007) · Molecular Cell · doi:10.1016/j.molcel.2007.05.017 · Cited by 1,365 · cited 1×
“p53 modulates the expression of numerous miRNA species, including miR34a,b and c [17,18].”
BackgroundSelf-citation
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Items 101–106 of 106
Extracellular and Intracellular Factors in Brain Cancer
Kanwore, K., Kambey, P. A., Guo, X., Abiola, A. A., Xia, Y., & Gao, D. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.699103
Nasif, S., & Roshdy, R. G. (2020) · Egyptian Journal of Pathology · doi:10.4103/egjp.egjp_9_21
Kojima, K., & Andreeff, M. (2015) · Wiley eBooks · doi:10.1002/9781118468678.ch36
Bao, X., Abdullaev, Z., Das, S., Zgonc, V., Ylaya, K., Pittaluga, S., Hewitt, S. M., Sedivy, J. M., Pack, S. J., Mackem, S., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.07.28.667174
“The oncogenic actions of MYC (1, 2) and the loss or mutation of tumor suppressor p53 (3-6) contribute to almost all human cancers.”
Development of microfluidic device for high content analysis of circulating tumor cells
Güneri, E. T. (2016) · theses.fr (ABES) · doi:10.70675/05968937zb93cz41cez8515zdf6113bf8d10
Implication de la voie p53 dans les syndromes d'insuffisance médullaire
Durand, R. (2020) · theses.fr (ABES) · doi:10.70675/6ccc120bz65f7z4c6czabf5z9bea26651b66
Metadata
- Authors
- Aylon, Y., & Oren, M.
- Affiliations
- Weizmann Institute of Science (IL)
- Corresponding author
- Oren, Moshe
- Venue
- Current Opinion in Genetics & Development
- Publisher
- Elsevier BV
- Published
- 2011-02
- Volume
- 21
- Issue
- 1
- Pages
- 86-92
- ISSN
- 0959-437X (ISSN-L)
- PMC
- PMC3059112
- OpenAlex
- W1988733824
- Cited by
- 106
- References
- 63
- Citations by year
- 2025: 4 · 2024: 3 · 2023: 2 · 2022: 5 · 2021: 6 · 2020: 10 · 2019: 6 · 2018: 6 · 2017: 2 · 2016: 8 · 2015: 7 · 2014: 14 · 2013: 6 · 2012: 18
- FWCI
- 1.15
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Current Opinion in Genetics & Development (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (R37 CA40099, R37CA040099)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- p53, p63, p73, tumor suppressor, transcription factors, non-coding RNA, RNA processing, tumor invasion, cellular metabolism, stem cell self-renewal
- MeSH terms
- Animals, Humans, Neoplasms, Stem Cells, Signal Transduction, Tumor Suppressor Protein p53, RNA, Untranslated
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