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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
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-citationmiR-34a repression of SIRT1 regulates apoptosis
Yamakuchi, M., Ferlito, M., & Lowenstein, C. J. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0801613105 · Cited by 1,362 · cited 1×
“Since Sirt1 is a negative regulator of p53, its downregulation by miR34a defines a positive feedback loop that amplifies p53 activity [20].”
BackgroundSuppression of induced pluripotent stem cell generation by the p53–p21 pathway
Hong, H., Takahashi, K., Ichisaka, T., Aoi, T., Kanagawa, O., Nakagawa, M., Okita, K., & Yamanaka, S. (2009) · Nature · doi:10.1038/nature08235 · Cited by 1,301 · cited 2×
“p53 in stem cells (SCs) and aging — two sides of the same coin? Recently, there has been a flourish of publications demonstrating that p53 deficiency facilitates reprogramming of differentiated cells into induced pluripotent stem (iPS) cells, closely resembling embryonic stem (ES) cells [42 ,43 ,44 ,45 ,46 ].”
BackgroundThe coordinate regulation of the p53 and mTOR pathways in cells
Feng, Z., Zhang, H., Levine, A. J., & Jin, S. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0502857102 · Cited by 1,235 · cited 1×
“Accordingly, p53 can positively affect autophagy, both by inhibiting mTOR activity and by transactivating proautophagic genes such as DRAM [14 ,15 ].”
BackgroundModulation of microRNA processing by p53
Suzuki, H. I., Yamagata, K., Sugimoto, K., Iwamoto, T., Kato, S., & Miyazono, K. (2009) · Nature · doi:10.1038/nature08199 · Cited by 1,158 · cited 1×
“p53 binding enhances recruitment of Drosha to target precursor miRNA and its processing activity towards a subset of miRNAs [26 ].”
BackgroundThe antioxidant function of the p53 tumor suppressor
Sablina, A. A., Budanov, A. V., Ilyinskaya, G. V., Agapova, L. S., Kravchenko, J. E., & Chumakov, P. M. (2005) · Nature Medicine · doi:10.1038/nm1320 · Cited by 1,137 · cited 2×
“Strikingly, dietary supplementation with the antioxidant N-acetylcysteine (NAC) completely abolished the incidence of lymphoma in p53 / mice [6 ], implicating p53’s antioxidant function as essential for its tumor suppressing action.”
BackgroundRegulation of autophagy by cytoplasmic p53
Tasdemir, E., Maiuri, M. C., Galluzzi, L., Vitale, I., Djavaheri-Mergny, M., D'Amelio, M., Criollo, A., Morselli, E., Zhu, C., Harper, F., et al. (2008) · Nature Cell Biology · doi:10.1038/ncb1730 · Cited by 1,132 · cited 1×
“Yet, p53 was also reported to inhibit autophagy, particularly under conditions where p53 is cytoplasmic [16 ].”
BackgroundLinking the p53 tumour suppressor pathway to somatic cell reprogramming
Kawamura, T., Suzuki, J., Wang, Y. V., Menendez, S., Morera, L. B., Raya, A., Wahl, G. M., & Belmonte, J. C. I. (2009) · Nature · doi:10.1038/nature08311 · Cited by 1,115
Brick by brick: metabolism and tumor cell growth
DeBerardinis, R. J., Sayed, N., Ditsworth, D., & Thompson, C. B. (2008) · Current Opinion in Genetics & Development · doi:10.1016/j.gde.2008.02.003 · Cited by 1,018
Chin, L., Artandi, S. E., Shen, Q., Tam, A., Lee, S.-L., Gottlieb, G. J., Greider, C. W., & DePinho, R. A. (1999) · Cell · doi:10.1016/s0092-8674(00)80762-x · Cited by 979 · cited 1×
“Germline deletion of p53 in mice with critically short telomeres spares damaged SCs from apoptosis and protracts their survival [53,54].”
BackgroundThe Ink4/Arf locus is a barrier for iPS cell reprogramming
Li, H., Collado, M., Villasante, A., Strati, K., Ortega, S., Cañamero, M., Blasco, M. A., & Serrano, M. (2009) · Nature · doi:10.1038/nature08290 · Cited by 968 · cited 2×
“p53 in stem cells (SCs) and aging — two sides of the same coin? Recently, there has been a flourish of publications demonstrating that p53 deficiency facilitates reprogramming of differentiated cells into induced pluripotent stem (iPS) cells, closely resembling embryonic stem (ES) cells [42 ,43 ,44 ,45 ,46 ].”
Backgroundp53 induces differentiation of mouse embryonic stem cells by suppressing Nanog expression
Lin, T., Chao, C., Saito, S., Mazur, S. J., Murphy, M. E., Appella, E., & Xu, Y. (2004) · Nature Cell Biology · doi:10.1038/ncb1211 · Cited by 859 · cited 2×
“Lin T, Chao C, Saito S, Mazur SJ, Murphy ME, Appella E, Xu Y: p53 induces differentiation of mouse embryonic stem cells by suppressing Nanog expression.”
BackgroundImmortalization eliminates a roadblock during cellular reprogramming into iPS cells
Utikal, J. S., Polo, J. M., Stadtfeld, M., Maherali, N., Kulalert, W., Walsh, R. M., Khalil, A., Rheinwald, J. G., & Hochedlinger, K. (2009) · Nature · doi:10.1038/nature08285 · Cited by 853 · cited 2×
“p53 in stem cells (SCs) and aging — two sides of the same coin? Recently, there has been a flourish of publications demonstrating that p53 deficiency facilitates reprogramming of differentiated cells into induced pluripotent stem (iPS) cells, closely resembling embryonic stem (ES) cells [42 ,43 ,44 ,45 ,46 ].”
Backgroundp53 represses c-Myc through induction of the tumor suppressor miR-145
Sachdeva, M., Zhu, S., Wu, F., Wu, H., Walia, V., Kumar, S. R., Elble, R. C., Watabe, K., & Mo, Y. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0808042106 · Cited by 841 · cited 2×
“Other miRs transactivated by p53 include miR-192, miR-215 [21] and miR-145 [22 ].”
BackgroundMutant p53 drives invasion by promoting integrin recycling
Muller, P. A. J., Caswell, P. T., Doyle, B., Iwanicki, M. P., Tan, E. H., Karim, S., Lukashchuk, N., Gillespie, D. A., Ludwig, R. L., Gosselin, P., et al. (2009) · Cell · doi:10.1016/j.cell.2009.11.026 · Cited by 796 · cited 2×
“It now emerges that the latter may be largely due to the inhibition of anti-invasive and anti-migratory effects of p63 by mutp53 [39 ,40 ].”
BackgroundA Mutant-p53/Smad Complex Opposes p63 to Empower TGFβ-Induced Metastasis
Adorno, M., Cordenonsi, M., Montagner, M., Dupont, S., Wong, C., Hann, B. C., Solari, A., Bobisse, S., Rondina, M. B., Guzzardo, V., et al. (2009) · Cell · doi:10.1016/j.cell.2009.01.039 · Cited by 794
Mutant p53 Gain-of-Function in CancerPreprint
Oren, M., & Rotter, V. (2009) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a001107 · Cited by 778 · cited 1×
“Mounting evidence indicates that such mutp53 proteins acquire cancer-promoting gain of function activities, including promotion of metastasis [38].”
BackgroundSelf-citationThe Tumor Suppressor p53 Regulates Polarity of Self-Renewing Divisions in Mammary Stem Cells
Cicalese, A., Bonizzi, G., Pasi, C. E., Faretta, M., Ronzoni, S., Giulini, B., Brisken, C., Minucci, S., Fiore, P. P. D., & Pelicci, P. G. (2009) · Cell · doi:10.1016/j.cell.2009.06.048 · Cited by 713 · cited 1×
“In a mouse model of ErbB2-driven breast cancer, cultured p53 / mammospheres were found enriched for self-renewing ‘SCs’ due to loss of p53 control over asymmetric cell division [58 ].”
Backgroundp53 regulates glucose metabolism through an IKK-NF-κB pathway and inhibits cell transformation
Kawauchi, K., Araki, K., Tobiume, K., & Tanaka, N. (2008) · Nature Cell Biology · doi:10.1038/ncb1724 · Cited by 660 · 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).”
BackgroundSenescence impairs successful reprogramming to pluripotent stem cells
Banito, A., Rashid, S. T., Acosta, J. C., Li, S., Pereira, C. F., Geti, I., Pinho, S., Silva, J. C., Azuara, V., Walsh, M., et al. (2009) · Genes & Development · doi:10.1101/gad.1811609 · Cited by 642 · cited 1×
“One possibility is that the iPS procedure indirectly causes DNA damage, driving p53 to activate a barrier of anti-proliferative senescence [47,48].”
BackgroundFeng, Z., Hu, W., de Stanchina, E., Teresky, A. K., Jin, S., Lowe, S., & Levine, A. J. (2007) · Cancer Research · doi:10.1158/0008-5472.can-06-4149 · Cited by 633 · cited 1×
“Perhaps not surprisingly, AMPK both activates and is activated by p53 in response to energetic stress [12,13].”
Backgroundp53 Regulates Hematopoietic Stem Cell Quiescence
Liu, Y., Elf, S. E., Miyata, Y., Sashida, G., Liu, Y., Huang, G., Di Giandomenico, S., Lee, J. M., Deblasio, A., Menendez, S., et al. (2009) · Cell Stem Cell · doi:10.1016/j.stem.2008.11.006 · Cited by 547 · cited 1×
“Current Opinion in Genetics & Development 2011, 21:86–92 accounting for their accelerated aging phenotype [60]; the same may hold for SCs of other tissues.”
Backgroundp53 controls cancer cell invasion by inducing the MDM2-mediated degradation of Slug
Wang, S.-P., Wang, W.-L., Chang, Y.-L., Wu, C.-T., Chao, Y.-C., Kao, S.-H., Yuan, A., Lin, C.-W., Yang, S.-C., Chan, W.-K., et al. (2009) · Nature Cell Biology · doi:10.1038/ncb1875 · Cited by 493 · cited 1×
“This inhibitory effect of p53 is partly mediated by Mdm2, which promotes the ubiquitination and degradation of Slug and Snail, pivotal transcription factors that drive tumor cell invasiveness [29,30].”
Backgroundp53-Responsive MicroRNAs 192 and 215 Are Capable of Inducing Cell Cycle Arrest
Braun, C. J., Zhang, X., Savelyeva, I., Wolff, S., Moll, U. M., Schepeler, T., Orntoft, T. F., Andersen, C. L., & Dobbelstein, M. (2008) · Cancer Research · doi:10.1158/0008-5472.can-08-1569 · Cited by 476 · cited 1×
“Other miRs transactivated by p53 include miR-192, miR-215 [21] and miR-145 [22 ].”
BackgroundDelayed ageing through damage protection by the Arf/p53 pathway
Matheu, A., Maraver, A., Klatt, P., Flores, I., Garcia-Cao, I., Borras, C., Flores, J. M., Viña, J., Blasco, M. A., & Serrano, M. (2007) · Nature · doi:10.1038/nature05949 · Cited by 466 · cited 1×
“That being said, other studies suggest an anti-aging effect of p53: transgenic mice with only a mild increase in p53 exhibit a reduced rate of age-related oxidative damage, more efficient clearing of DNA-damaged cells and enhanced longevity [61].”
ResultLi, N., Fu, H., Tie, Y., Hu, Z., Kong, W., Wu, Y., & Zheng, X. (2008) · Cancer Letters · doi:10.1016/j.canlet.2008.09.035 · Cited by 426 · cited 1×
“Furthermore, p53-regulated miRNAs such as miR-34a, which downregulates c-Met, Notch1 and Jagged1, also contribute to p53’s ability to repress migration and invasion [32,33].”
Backgroundp63 regulates an adhesion programme and cell survival in epithelial cells
Carroll, D. K., Carroll, J. S., Leong, C., Cheng, F., Brown, M. A., Mills, A. A., Brugge, J. S., & Ellisen, L. W. (2006) · Nature Cell Biology · doi:10.1038/ncb1420 · Cited by 403 · cited 1×
“Like its cousin p53, p63 also modulates adhesion, migration and invasion [34–37].”
BackgroundThe regulation of energy metabolism and the IGF-1/mTOR pathways by the p53 protein
Feng, Z., & Levine, A. J. (2010) · Trends in Cell Biology · doi:10.1016/j.tcb.2010.03.004 · Cited by 373 · cited 2×
“Besides responding to glucose levels, mTOR senses changes in the availability of amino acids, ATP/AMP and growth factors [11].”
Backgroundp53-independent upregulation of miR-34a during oncogene-induced senescence represses MYC
Christoffersen, N. R., Shalgi, R., Frankel, L. B., Leucci, E., Lees, M., Klausen, M., Pilpel, Y., Nielsen, F. C., Oren, M., & Lund, A. H. (2010) · Cell Death & Differentiation · doi:10.1038/cdd.2009.109 · Cited by 352 · cited 1×
“For example, miR-34a contributes to p53-dependent apoptosis, as well as cell cycle arrest and senescence [17–19].”
BackgroundSelf-citationp53-Mediated Hematopoietic Stem and Progenitor Cell Competition
Bondar, T., & Medzhitov, R. (2010) · Cell Stem Cell · doi:10.1016/j.stem.2010.03.002 · Cited by 342 · cited 1×
“Similarly, elegant in vivo competition experiments show that p53-deficient mouse hematopoietic stem cells (HSCs) have improved repopulation capacity in transplantation assays, while the outcompeted p53-proficient SCs acquire senescence-like features [56].”
BackgroundMilyavsky, M., Gan, O. I., Trottier, M., Komosa, M., Tabach, O., Notta, F., Lechman, E. R., Hermans, K. G., Eppert, K., Konovalova, Z., et al. (2010) · Cell stem cell · doi:10.1016/j.stem.2010.05.016 · Cited by 289 · cited 1×
“Surprisingly, recent analysis of human HSCs [57 ] reveals a strikingly different picture.”
BackgroundFeng, Z., Hu, W., Teresky, A. K., Hernando, E., Cordon-Cardo, C., & Levine, A. J. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0708043104 · Cited by 264 · cited 1×
“Interestingly, in mice and humans, p53 activity declines with age [62], probably contributing to the concomitant increase in cancer frequency.”
BackgroundRegulation of Apoptosis and Differentiation by p53 in Human Embryonic Stem Cells
Qin, H., Yu, T., Qing, T., Liu, Y., Zhao, Y., Cai, J., Li, J., Song, Z., Qu, X., Zhou, P., et al. (2006) · Journal of Biological Chemistry · doi:10.1074/jbc.m610464200 · Cited by 245 · cited 1×
“Interestingly, p53 was reported to protect mouse ES cells from DNA damage not by exerting cell cycle arrest or apoptosis, but by inducing differentiation via suppression of the SC-specific genes Nanog [51] and Oct4 [52].”
BackgroundPang, R. T. K., Leung, C. O. N., Ye, T.-M., Liu, W., Chiu, P. C. N., Lam, K. K. W., Lee, C., & Yeung, W. S. B. (2010) · Carcinogenesis · doi:10.1093/carcin/bgq066 · Cited by 245 · cited 1×
“Furthermore, p53-regulated miRNAs such as miR-34a, which downregulates c-Met, Notch1 and Jagged1, also contribute to p53’s ability to repress migration and invasion [32,33].”
BackgroundLoss of p53 promotes RhoA–ROCK-dependent cell migration and invasion in 3D matrices
Gadéa, G., de Toledo, M., Anguille, C., & Roux, P. (2007) · The Journal of Cell Biology · doi:10.1083/jcb.200701120 · Cited by 244 · cited 1×
“Loss of p53 augments cancer cell invasion [27]; conversely, p53 activation suppresses migration and invasion [28].”
BackgroundBarbieri, C. E., Tang, L. J., Brown, K., & Pietenpol, J. A. (2006) · Cancer Research · doi:10.1158/0008-5472.can-06-2020 · Cited by 232 · cited 1×
“Like its cousin p53, p63 also modulates adhesion, migration and invasion [34–37].”
BackgroundSuppression of induced pluripotent stem cell generation by the p53-p21 pathway
洪, 炫. (2012) · Medical Entomology and Zoology · Cited by 198
p53 loss promotes acute myeloid leukemia by enabling aberrant self-renewalPreprint
Zhao, Z., Zuber, J. A., Díaz-Flores, E., Lintault, L., Kogan, S. C., Shannon, K., & Lowe, S. W. (2010) · Genes & Development · doi:10.1101/gad.1940710 · Cited by 175 · cited 1×
“In the hematopoietic system, K-Ras activation instigates a burst of hyperproliferation, but subsequent p53-driven terminal differentiation of stem and progenitor cells provides a p53-dependent barrier against limitless proliferation of undifferentiated leukemia-initiating cells [59].”
BackgroundSarig, R., Rivlin, N., Brosh, R., Bornstein, C., Kamer, I., Ezra, O., Molchadsky, A., Goldfinger, N., Brenner, O. J., & Rotter, V. (2010) · The Journal of Experimental Medicine · doi:10.1084/jem.20100797 · Cited by 162 · cited 2×
“p53 in stem cells (SCs) and aging — two sides of the same coin? Recently, there has been a flourish of publications demonstrating that p53 deficiency facilitates reprogramming of differentiated cells into induced pluripotent stem (iPS) cells, closely resembling embryonic stem (ES) cells [42 ,43 ,44 ,45 ,46 ].”
Backgroundp53 is balancing development, differentiation and de-differentiation to assure cancer prevention
Molchadsky, A., Rivlin, N., Brosh, R., Rotter, V., & Sarig, R. (2010) · Carcinogenesis · doi:10.1093/carcin/bgq101 · Cited by 161 · cited 1×
“Alternatively, explicit pro-differentiation effects of p53 [49] might actively inhibit the iPS program.”
BackgroundA pivotal role for p53: balancing aerobic respiration and glycolysis
Ma, W., Sung, H. J., Park, J., Matoba, S., & Hwang, P. M. (2007) · Journal of Bioenergetics and Biomembranes · doi:10.1007/s10863-007-9083-0 · Cited by 153 · 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).”
Backgroundp53 and the Li-Fraumeni syndrome
Malkin, D. M. (1993) · Cancer Genetics and Cytogenetics · doi:10.1016/0165-4608(93)90233-c · Cited by 153 · cited 1×
“Introduction Humans with germline p53 mutations are affected by the Li-Fraumeni syndrome, characterized by very high cancer susceptibility [1,2].”
Backgroundp53‐repressed miRNAs are involved with E2F in a feed‐forward loop promoting proliferation
Brosh, R., Shalgi, R., Liran, A., Landan, G., Korotayev, K., Nguyen, G. H., Enerly, E., Johnsen, H., Buganim, Y., Solomon, H., et al. (2008) · Molecular Systems Biology · doi:10.1038/msb.2008.65 · Cited by 153 · cited 2×
“Current Opinion in Genetics & Development 2011, 21:86–92 A cluster of cancer-associated miRNAs, including miR106b/93/25 and others, is repressed by p53 in an E2F1mediated manner [23 ].”
BackgroundSelf-citationTumourigenesis associated with the p53 tumour suppressor gene
Chang, F., Syrjänen, S., Tervahauta, A. I., & Syrjänen, K. J. (1993) · British Journal of Cancer · doi:10.1038/bjc.1993.404 · Cited by 117 · cited 1×
“Introduction Humans with germline p53 mutations are affected by the Li-Fraumeni syndrome, characterized by very high cancer susceptibility [1,2].”
BackgroundInduced pluripotent stem cells and senescence: learning the biology to improve the technology
Banito, A., & Gil, J. (2010) · EMBO Reports · doi:10.1038/embor.2010.47 · Cited by 111 · cited 1×
“One possibility is that the iPS procedure indirectly causes DNA damage, driving p53 to activate a barrier of anti-proliferative senescence [47,48].”
Backgroundp53 inhibits tumor cell invasion via the degradation of snail protein in hepatocellular carcinoma
Lim, S., Kim, H., & Jung, G. (2010) · FEBS Letters · doi:10.1016/j.febslet.2010.04.006 · Cited by 102 · cited 1×
“This inhibitory effect of p53 is partly mediated by Mdm2, which promotes the ubiquitination and degradation of Slug and Snail, pivotal transcription factors that drive tumor cell invasiveness [29,30].”
BackgroundSankpal, N. V., Willman, M. W., Fleming, T. P., Mayfield, J. D., & Gillanders, W. E. (2009) · Cancer Research · doi:10.1158/0008-5472.can-08-2708 · Cited by 91 · cited 1×
“In addition, p53 inhibits invasion by modulation of cell adhesion proteins such as EpCAM [31].”
BackgroundBegus-Nahrmann, Y., Lechel, A., Obenauf, A. C., Nalapareddy, K., Peit, E., Hoffmann, E., Schlaudraff, F., Liss, B., Schirmacher, P., Kestler, H., et al. (2009) · Nature Genetics · doi:10.1038/ng.426 · Cited by 88 · cited 1×
“Germline deletion of p53 in mice with critically short telomeres spares damaged SCs from apoptosis and protracts their survival [53,54].”
BackgroundFlores, I., & Blasco, M. A. (2009) · PLoS ONE · doi:10.1371/journal.pone.0004934 · Cited by 83 · cited 12×
“Germline deletion of p53 in mice with critically short telomeres spares damaged SCs from apoptosis and protracts their survival [53,54].”
BackgroundInfluentialDong, P., Xu, Z., Jia, N., Li, D., & Feng, Y. (2009) · Molecular Cancer · doi:10.1186/1476-4598-8-103 · Cited by 75 · cited 1×
“The outcome of this activity of mutp53 is repression of anti-invasion genes [39 ], enhancement of integrin and EGF receptor (EGFR) recycling [40 ] driving activation of the EGFR pathway [41], and eventual promotion of metastasis.”
p63 contributes to cell invasion and migration in squamous cell carcinoma of the head and neck
Gu, X., Coates, P. J., Boldrup, L., & Nylander, K. (2008) · Cancer Letters · doi:10.1016/j.canlet.2007.12.011 · Cited by 49 · cited 1×
“Like its cousin p53, p63 also modulates adhesion, migration and invasion [34–37].”
BackgroundRegulation of VDR by ΔNp63α is associated with inhibition of cell invasion
Kommagani, R., Leonard, M. K., Lewis, S., Romano, R., Sinha, S., & Kadakia, M. (2009) · Journal of Cell Science · doi:10.1242/jcs.049619 · Cited by 47
Moran, D. M., & Maki, C. G. (2010) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-09-1220 · Cited by 35 · cited 1×
“Loss of p53 augments cancer cell invasion [27]; conversely, p53 activation suppresses migration and invasion [28].”
Backgroundp53 Regulation Orchestrates the TGF-β Response
Piccolo, S. (2008) · Cell · doi:10.1016/j.cell.2008.05.013 · Cited by 27 · cited 1×
“Indeed, in frog development, p53 interacts with Smad transcriptional regulators to direct embryonic germ layer specification [50].”
Cited by
Sorted by citations
Ferroptosis as a p53-mediated activity during tumour suppression
Jiang, L., Kon, N., Li, T., Wang, S.-J., Su, T., Hibshoosh, H., Baer, R., & Gu, W. (2015) · Nature · doi:10.1038/nature14344 · Cited by 3,398
Rivlin, N., Brosh, R., Oren, M., & Rotter, V. (2011) · Genes & Cancer · doi:10.1177/1947601911408889 · Cited by 1,033
“The many roles of p53 as a tumor suppressor include the ability to induce cell cycle arrest, DNA repair, senescence, and apoptosis, to name only a few.(6) Indeed, TP53 mutations were reported to occur in almost every type of cancer at rates varying between 10% (e.”
BackgroundSelf-citationInterleukin-1 Beta—A Friend or Foe in Malignancies?
Bent, R., Moll, L., Grabbe, S., & Bros, M. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19082155 · Cited by 475
“p53 is known to maintain genomic integrity through apoptosis regulation despite DNA damage or instability and also regulates inflammation [255].”
BackgroundTumour-associated mutant p53 drives the Warburg effect
Zhang, C., Liu, J., Liang, Y., Wu, R., Zhao, Y., Hong, X., Lin, M., Yu, H., Liu, L., Levine, A. J., et al. (2013) · Nature Communications · doi:10.1038/ncomms3935 · Cited by 434
“Recent studies have shown that regulating energy metabolism is a critical function of wtp53 in tumor suppression 12, 13, 17, 18 .”
TP53 Mutations in Human Cancer: Database Reassessment and Prospects for the Next Decade
Leroy, B., Anderson, M., & Soussi, T. (2014) · Human Mutation · doi:10.1002/humu.22552 · Cited by 422
“However, several recent reviews are available [Aylon and Oren, 2011; Levine et al., 2011; Berkers et al., 2013].”
Background
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
