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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]
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“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
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BackgroundSelf-citation
Cited by
Sorted by citations
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“p53 and its homologues p63 and p73 control cell cycle progression, apoptosis, senescence, differentiation and stemness.(101) p63 and p73 exist as full-sized proteins (TAp63 and TAp73) or truncated versions (DNp63 and DNp73), which lack transcriptional activation domains.”
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Shang, M., Soon, R. H., Lim, C. T., Khoo, B. L., & Han, J. (2019) · Lab on a Chip · doi:10.1039/c8lc00970h · Cited by 227
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“In nearly 50% of human cancers, p53 is found to be mutated, and in many of the remaining cases, where the WT allele is retained, other components in the p53 pathway are defected [13].”
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“During the past decade, compelling evidence revealed that p53, as a master transcription factor and a crucial sensor of stress, participates in the regulation of a plethora of physiological processes throughout the entire lifespan of the organism, including stem cell state, development, tissue homeostasis, metabolism,…”
BackgroundWerner, H. (2011) · Oncogene · doi:10.1038/onc.2011.447 · Cited by 128
“…wild-type p53 arrests cell cycle progression at the G1 phase, hence enabling damaged DNA to be repaired before the replicative phase. p53 can, alternatively, elicit an apoptotic program and multiple target genes of p53 Oncogene have been identified (Aylon and Oren, 2011; Tang et al., 2011).”
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Alterations of theTP53Gene in Gastric and Esophageal Carcinogenesis
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“In addition to the wellknown effect of p53 in maintaining genomic integrity despite DNA damage or instability through apoptosis regulation [11], p53 is known to function in regulation of inflammation [12].”
BackgroundTumor suppressor p53 negatively regulates glycolysis stimulated by hypoxia through its target RRAD
Zhang, C., Liu, J., Wu, R., Liang, Y., 林美华, Liu, J., Chan, C. S., Hu, W., & Feng, Z. (2014) · Oncotarget · doi:10.18632/oncotarget.2137 · Cited by 101
“Recently, p53 has been reported to negatively regulate aerobic glycolysis under normoxic conditions through the regulation of many different genes and different mechanisms [9-12].”
BackgroundLow-dose radiation exposure induces a HIF-1-mediated adaptive and protective metabolic response
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Porter, J. R., Fisher, B. E., & Batchelor, E. (2016) · Cell Systems · doi:10.1016/j.cels.2016.03.006 · Cited by 90
“…genes involved in a range of cellular stress responses including apoptosis, cell cycle arrest, senescence, DNA repair, and changes in metabolism (Aylon and Oren, 2011; Riley et al., 2008). p53 pulsing directly impacts p53 function: altering p53 dynamics by pharmacologically inhibiting p53…”
BackgroundZampetidis, C., Galanos, P., Angelopoulou, A., Zhu, Y., Polyzou, A., Karamitros, T., Kotsinas, A., Lаgopati, N., Mourkioti, I., Mirzazadeh, R., et al. (2021) · Molecular Cell · doi:10.1016/j.molcel.2021.10.017 · Cited by 94
Alternative splicings on p53, BRCA1 and PTEN genes involved in breast cancer
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The p53 control of apoptosis and proliferation: lessons from Drosophila
Mollereau, B., & Ma, D. (2014) · APOPTOSIS · doi:10.1007/s10495-014-1035-7 · Cited by 71
“In addition, other types of cellular stresses such as starvation and metabolic stress also activate p53 response pathways such as the antioxidant response and autophagy [3–6].”
BackgroundArhGAP30 promotes p53 acetylation and function in colorectal cancer
Wang, J., Qian, J., Hu, Y., Kong, X., Chen, H., Shi, Q., Jiang, L., Wu, C., Zou, W., Chen, Y., et al. (2014) · Nature Communications · doi:10.1038/ncomms5735 · Cited by 69
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Melanocytes: A Window into the Nervous System
Yaar, M., & Park, H. (2011) · Journal of Investigative Dermatology · doi:10.1038/jid.2011.386 · Cited by 72
“Cellular stresses including DNA damage activate p53, leading to cell cycle arrest, DNA damage repair, senescence, and/or apoptosis, depending on the extent of the damage (Aylon and Oren, 2011).”
BackgroundSTEAP3 Affects Ferroptosis and Progression of Renal Cell Carcinoma Through the p53/xCT Pathway
Ye, C. L., Du, Y., Yu, X., Chen, Z. Y., Wang, L., Zheng, Y. F., & Liu, X. H. (2022) · Technology in Cancer Research & Treatment · doi:10.1177/15330338221078728 · Cited by 64
Liang, Y., Zhang, D., Zheng, T., Yang, G., Wang, J., Meng, F., Liu, Y., Zhang, G., Zhang, L., Han, J., et al. (2020) · Oncogenesis · doi:10.1038/s41389-020-0242-z · Cited by 63
Werner, H., & Sarfstein, R. (2014) · Growth Hormone & IGF Research · doi:10.1016/j.ghir.2014.03.006 · Cited by 57
“p53 can, alternatively, elicit an apoptotic program and several p53-target genes have been identified [26].”
BackgroundTargeting Loss of Heterozygosity: A Novel Paradigm for Cancer Therapy
Zhang, X., & Sjöblom, T. (2021) · Pharmaceuticals · doi:10.3390/ph14010057 · Cited by 58
“1 is one of the most frequent genetic alterations leading to human cancers [78,79].”
BackgroundA comprehensive study of p53 protein
Patil, M. R., & Bihari, A. (2022) · Journal of Cellular Biochemistry · doi:10.1002/jcb.30331 · Cited by 57
“are among other things involved.(80) In human cancer, TP53 is typically identified to be inappropriately mutated, with one nucleotide being replaced by another, as are most tumor‐suppressing genes such as RB, APC, or BRCA.”
BackgroundCyclin D mediates tolerance of genome-doubling in cancers with functional p53
Crockford, A., Zalmas, L., Gronroos, E. C., Dewhurst, S. M., McGranahan, N., Cuomo, M. E., Encheva, V., Snijders, A. P., Begum, J., Purewal, S., et al. (2016) · Annals of Oncology · doi:10.1093/annonc/mdw612 · Cited by 54
“Although mutations in TP53 are significantly associated with genome-doubling in tumours [6, 7], we show that a large proportion of genomedoubled tumours have a functional p53 axis and no other known genetic aberrations that could permit tetraploidization.”
BackgroundRegulation of skin aging and heart development by TAp63
Paris, M., Rouleau, M., Pucéat, M., & Aberdam, D. (2011) · Cell Death and Differentiation · doi:10.1038/cdd.2011.181 · Cited by 58
“p63 belongs to the p53 family of transcription factors, together with p53 and p73.(1) By encoding two different N-termini (TA and DN) and multiple C-termini by alternative splicing, the TP63 gene generates multiple-protein isoforms.”
BackgroundCraene, B. D., Denecker, G., Vermassen, P., Taminau, J., Mauch, C., Derore, A., Jonkers, J., Fuchs, E. V., & Berx, G. (2013) · Cell Death and Differentiation · doi:10.1038/cdd.2013.148 · Cited by 54
“The tumour-suppressor p53 has an integral role in cellular responses to DNA damage, but there is also substantial evidence that p53 deficiency facilitates reprogramming of differentiated cells.(34) Moreover, p53 loss rescues epidermal stem cell function in telomerase-deficient mice.”
BackgroundRole of the GH-IGF1 system in progression of cancer.
Werner, H., & Laron, Z. (2020) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2020.111003 · Cited by 42
PCDH10, a novel p53 transcriptional target in regulating cell migration
Shi, D., Murty, V. V. V. S., & Gu, W. J. (2015) · Cell Cycle · doi:10.1080/15384101.2015.1004935 · Cited by 51
“In fact, a growing number of non-canonical p53 target genes have been added to the p53 transcription program, and these genes encode for proteins ranging over a broad spectrum of cellular functions in cell metabolism, stem cell differentiation, tumor cell invasion, and yet unknown functions.(1) The aberrantly increase…”
BackgroundAlternative Splicing in Breast Cancer and the Potential Development of Therapeutic Tools
Martínez-Montiel, N., Anaya-Ruı́z, M., Pérez-Santos, M., & Martínez-Contreras, R. D. (2017) · Genes · doi:10.3390/genes8100217 · Cited by 48
Denisenko, T. V., Pivnyuk, A. D., & Zhivotovsky, B. (2018) · Cancers · doi:10.3390/cancers10050148 · Cited by 51
“Interestingly, p53 was also shown to play a crucial role in the control of cell migration and invasion [109,111].”
BackgroundGuo, G., & Cui, Y. R. (2015) · Journal for ImmunoTherapy of Cancer · doi:10.1186/s40425-015-0053-5 · Cited by 47
“Even though p53 is the best studied gene as the result of 30 years extensive research, our comprehension and appreciation of its complexity in regulating many crucial biological processes are far from complete [4,9,16-18].”
BackgroundModeling the Basal Dynamics of P53 System
Sun, T., Yang, W., Liu, J., & Shen, P. (2011) · PLoS ONE · doi:10.1371/journal.pone.0027882 · Cited by 43
TSPAN2 Is Involved in Cell Invasion and Motility during Lung Cancer Progression
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The emerging functions of the p53-miRNA network in stem cell biology
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“The dual functions of p53 to promote or repress ES cell differentiation are reminiscent of its pro- and anti-apoptotic roles in somatic cells.(24) In response to mild, reparable damage in somatic cells, p53 primarily triggers growth arrest, allowing DNA repaired cells to re-enter normal cell cycle; however, p53 activa…”
BackgroundFleury, H., Communal, L., Carmona, E., Portelance, L., Arcand, S. L., Rahimi, K., Tonin, P. N., Provencher, D. M., & Mes‐Masson, A. (2015) · Genes & Cancer · doi:10.18632/genesandcancer.76 · Cited by 36
“The p53 protein functions as a transcriptional factor with a crucial role in cellular stress response (reviewed in [63-65]).”
Role of the promyelocytic leukaemia protein in cell death regulation
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Zhao, Q., Fan, J., Wei, H., Li, L., & Wu, M. (2012) · SpringerPlus · doi:10.1186/2193-1801-1-65 · Cited by 33
“Activated p53 transcribes a number of genes to induce cell cycle arrest, apoptosis, and senescence, all of which help in suppressing tumorigenesis (Vousden and Prives 2009; Speidel 2010; Aylon and Oren 2011).”
Özdemir, E. S., Halakou, F., Nussinov, R., Gürsoy, A., & Keskin, Ö. (2018) · Methods in molecular biology · doi:10.1007/978-1-4939-8955-3_1 · Cited by 34
p53 balances between tissue hierarchy and anarchy
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“The tumor suppressor activity of p53 is mainly attributed to its ability to modulate transcription of genes that are involved in numerous cellular processes, such as cell cycle arrest, apoptosis, senescence, DNA repair and differentiation (Chipuk and Green, 2006; Levine and Oren, 2009; Aylon and Oren, 2011; Rivlin et…”
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“In its wild-type form, p53 is a master regulator of diverse cellular processes such as cell apoptosis, cycle arrest, metabolism, and metastasis [43].”
Backgroundp53 in cell invasion, podosomes, and invadopodia
Mak, A. S. (2014) · Cell Adhesion & Migration · doi:10.4161/cam.27841 · Cited by 28
“A survey of p53-regulated human genes reveals many regulators of cell migration and invasion, including proteins involved in endothelial-mesenchymal-transition (EMT) and the extra cellular matrix (ECM) composition and invasion, growth factor receptors, and adhesion signaling.(1,16,17) Some of these migration and invas…”
Kim, J., Chang, J. W., Park, J. K., & Hwang, S. (2012) · Cancer Biology & Therapy · doi:10.4161/cbt.20081 · Cited by 27
Dioufa, N., Chatzistamou, I., Farmaki, E., Papavassiliou, A. G., & Kiaris, H. (2012) · Experimental Biology and Medicine · doi:10.1258/ebm.2012.012140 · Cited by 26
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“The murine/human double minute 2 (MDM2/HDM2) is an E3 ubiquitin ligase that promotes p53 degradation and forms a negative feedback loop that controls p53 activity (Aylon and Oren, 2007; Chen et al., 2010).”
BackgroundRecent progress in genetics of aging, senescence and longevity: focusing on cancer-related genes
Berman, A. E., Leontieva, O. V., Natarajan, V., McCubrey, J. A., Demidenko, Z. N., & Nikiforov, M. A. (2012) · Oncotarget · doi:10.18632/oncotarget.889 · Cited by 24
Overexpression of MCPH1 inhibits the migration and invasion of lung cancer cells
Wu, X., Liu, W., Liu, X., Ai, Q., & Yu, J. (2018) · OncoTargets and Therapy · doi:10.2147/ott.s156102 · Cited by 22
“In addition, it has been reported that p53 may suppress the EMT via the p53/Mdm2 pathway, and MCPH1 can regulate p53 protein.(17,18) Therefore, we measured the cellular levels of these proteins after MCPH1 overexpression in A549 cells.”
Backgroundp53 controls CDC7 levels to reinforce G1 cell cycle arrest upon genotoxic stress
Tudzarova, S., Mulholland, P. J., Dey, A., Stoeber, K., Okorokov, A. L., & Williams, G. H. (2016) · Cell Cycle · doi:10.1080/15384101.2016.1231281 · Cited by 23
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Disease association of human tumor suppressor genes
Das, A. B. (2019) · Molecular Genetics and Genomics · doi:10.1007/s00438-019-01557-9 · Cited by 16
Genome-wide analysis of the p53 gene regulatory network in the developing mouse kidney
Li, Y., Liu, J., McLaughlin, N., Bachvarov, D. R., Saifudeen, Z. R., & El-Dahr, S. S. (2013) · Physiological Genomics · doi:10.1152/physiolgenomics.00113.2013 · Cited by 16
“, oxidative and glycolytic pathways for energy generation and glucose homeostasis (3, 4, 6, 19, 42).”
BackgroundAnitha, S., Digumarti, R., Waliyar, F., Sudini, H., Parveen, M., Rao, R., & Kumar, P. L. (2014) · Mutation Research/Genetic Toxicology and Environmental Mutagenesis · doi:10.1016/j.mrgentox.2013.12.011 · Cited by 16
“The role of TP53 as a tumoursuppressor gene includes the ability to induce cell cycle arrest, DNA repair, senescence, and apoptosis [20].”
BackgroundPayandeh, M., Sadeghi, M., Sadeghi, E., & Madani, S.-H. (2016) · Asian Pacific Journal of Cancer Prevention · doi:10.7314/apjcp.2015.17.3.1261 · Cited by 15
Vuong, L., Brobst, D. E., Saadi, A., Ivanovic, I., & Al‐Ubaidi, M. R. (2012) · Investigative Ophthalmology & Visual Science · doi:10.1167/iovs.11-8681 · Cited by 13
“The p53 tumor suppressor plays a critical role in regulating DNA damage repair, cell cycle progression, apoptosis, and autophagy.(1) It is also involved in the regulation of significant physiological steps during development, aging, and metabolism (for review, see ref.”
BackgroundLucchesi, C. A., Zhang, J., Gao, M., Shaw, J. T., & Chen, X. (2023) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-22-0627 · Cited by 12
Chang, L.-J., & Eastman, A. R. (2012) · Cancer Biology & Therapy · doi:10.4161/cbt.21047 · Cited by 12
“In many of the remaining 50%, the function of the retained wild-type p53 protein is compromised by deregulation of upstream or downstream components of the p53 pathway.(5) Although these p53-defective cancer cells are more resistant to p53-induced apoptosis, they have a dysfunctional G 1 checkpoint because of failure…”
BackgroundTomas, F., Roux, P., & Gire, V. (2024) · Cell Death and Disease · doi:10.1038/s41419-024-07213-4 · Cited by 11
“Upon DNA damage, p53 is rapidly stabilized and activates the transcription of genes involved in many responses, ranging from transient cell cycle arrest and DNA repair, to terminal outcomes, such as senescence and apoptosis [2, 3].”
Ferreira, W. A. S., Burbano, R. M. R., Pessoa, C. D. Ó., Harada, M. L., Borges, B. D. N., & de Oliveira, E. H. C. (2020) · Anti-Cancer Agents in Medicinal Chemistry · doi:10.2174/1871520620666200203160117 · Cited by 10
Alaee, M., Padda, A., Mehrabani, V., Churchill, L., & Pasdar, M. (2016) · Oncotarget · doi:10.18632/oncotarget.8616 · Cited by 11
“These effects are mediated by the p53 regulation of expression of various tumor suppressors, signaling molecules and oncogenic and tumor suppressor miRNAs [32-40].”
BackgroundHainaut, P. L., Wiman, K. G., & Olivier, M. (2012) · Springer eBooks · doi:10.1007/978-1-4614-3676-8 · Cited by 10
“Due to the presence of internal promoters and/or alternative splicing mechanisms, TP63 and TP73 encode two different classes of protein isoforms: those containing an N-terminal transactivation (TA) domain, similar to the one of p53, and those that lack this transactivation domain, commonly termed Delta-N isoforms.”
BackgroundCDKL3 Targets ATG5 to Promote Carcinogenesis of Esophageal Squamous Cell Carcinoma
Zhou, S., Zhang, M., Chao Hui, Z. H. O. U., Wang, W., Yang, H., & Ye, W. (2020) · Frontiers in Oncology · doi:10.3389/fonc.2020.01602 · Cited by 10
“Wild type p53 considered as a key regulator in many cell-fate-determining processes and is mutated in nearly 50% of human tumors (25).”
BackgroundLiu, X., Wang, J., Wu, L., Trinh, B., & Tsai, R. Y. L. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25115992 · Cited by 9
Ci, X., Yu, Z., Tang, W., Tu, Q., Jiang, P., Xue, X., Saunders, N. A., Zhang, L., Zhu, X., & Zhao, K. (2020) · Applied Microbiology and Biotechnology · doi:10.1007/s00253-020-10492-4 · Cited by 11
Alzaidi, M. A., Arab, H. A., Amanpour, S., Shirkoohi, R., Muhammadnejad, S., & Sasani, F. (2018) · Journal of Gastrointestinal Cancer · doi:10.1007/s12029-017-0050-7 · Cited by 8
“There is evidence that during the process of DNA damage induced by different degradation factors, some genes are expressed to repair the injury [32].”
BackgroundTP53: Coordinator of the Processes That Underlie the Hallmarks of Cancer
Hainaut, P. L. (2012) · Springer eBooks · doi:10.1007/978-1-4614-3676-8_1 · Cited by 10
Progress and challenges in understanding the regulation and function of p53 dynamics
Yang, Z., Hanson, R. L., & Batchelor, E. (2021) · Biochemical Society Transactions · doi:10.1042/bst20210148 · Cited by 7
The Biological Function and Clinical Significance of miR-886-5p in Multiple Myeloma
Xiang, P., Liu, Y., Liu, L., Lin, Q., Liu, X., Zhang, H., Xu, J., & Fang, B. (2019) · Acta Haematologica · doi:10.1159/000499620 · Cited by 7
Xu, C., Yang, X., Wang, Y., Ding, N., Han, R., Sun, Y., & Wang, Y. (2017) · Cancer Gene Therapy · doi:10.1038/cgt.2017.17 · Cited by 6
Association of EGF and p53 gene polymorphisms and colorectal cancer risk in the Slovak population
Mahmood, S., Sivoňová, M. K., Matáková, T., Dobrota, D., Wsólová, L., Dzian, A., & Mistuna, D. (2014) · Open Medicine · doi:10.2478/s11536-013-0300-4 · Cited by 6
Les deux visages de p63, Janus de la famille p53
de Fromentel, C. C., Aberdam, É., & Aberdam, D. (2012) · médecine/sciences · doi:10.1051/medsci/2012284015 · Cited by 5
“La notion de famille TP53 a été proposée il y a une quinzaine d’année, après la découverte de deux gènes homologues TP63 et TP73 [1].”
Bi, Y.-H., Wang, J., Guo, Z., & Jia, K. (2022) · Journal of Pain Research · doi:10.2147/jpr.s385228 · Cited by 6
“TP53 downstream target genes, triggering cell cycle arrest and apoptosis.(48,49) The TP53 family regulates NF-κB/REL expression, which in turn promotes proliferative inflammation and the malignant phenotype of head and neck squamous carcinomas.”
BackgroundAtox1-cyclin D1 loop activity is critical for survival of tumor cells with inactivated TP53
Kuchur, O. A., Pogodaeva, S. S., Shcherbakova, A. V., & Tsymbal, S. A. (2024) · Bioscience Reports · doi:10.1042/bsr20240389 · Cited by 6
Family matters: sibling rivalry and bonding between p53 and p63 in cancer
Romano, R., & Sinha, S. (2014) · Experimental Dermatology · doi:10.1111/exd.12356 · Cited by 6
Reddy, V. R., Annamalai, T., Narayanan, V., & Ramanathan, A. (2015) · Asian Pacific Journal of Cancer Prevention · doi:10.7314/apjcp.2015.16.4.1599 · Cited by 5
Lucchesi, C. A., Zhang, J., Vasilatis, D. M., Yip, E., & Chen, X. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2022.893062 · Cited by 5
“Functionally, activated p53 stimulates multiple antiproliferative mechanisms by modulating expression of genes involved in DNA repair, cell cycle arrest, apoptosis, and senescence (6).”
BackgroundAssociation Between TP53 Mutation and Prognosis in Wilms Tumor: A Meta-Analysis
Li, L., Rongdong, H., He, S., Yingquan, K., Xu, H., Lin, S., Tang, K., & Xu, D. (2020) · Fetal and Pediatric Pathology · doi:10.1080/15513815.2020.1725937 · Cited by 4
“The TP53 gene encodes p53 protein in human, which is a transcription factor and plays a role in apoptosis, cell cycle arrest, DNA repair, and senescence [29,30].”
BackgroundStatus of p53 and p27KIP1 in Iranian Patients With Oral Squamous Cell Carcinoma
Etemad‐Moghadam, S., Keyhani, A., Yazdani, K., & Alaeddini, M. (2015) · Iranian Red Crescent Medical Journal · doi:10.5812/ircmj.19359 · Cited by 5
“In addition, p53 has been recently shown to affect a variety of cellular features and processes, including cellular metabolism, noncoding ribonucleic acids (RNAs), tumor cell invasion, and possibly “reprogramming of differentiated cells into induced pluripotent stem cells” (5).”
BackgroundFei, J.-W., & de Villiers, E. (2012) · PLoS ONE · doi:10.1371/journal.pone.0035540 · Cited by 4
“Mutant p53 binds to promoters to form transcriptionally active complexes, thereby gaining function [24,25].”
BackgroundNiknejad, A., Esmaealzadeh, N., Peyrovinasab, A., Sirouskabiri, S., Gholami, M., Pasha, A. V. K., Shahri, S., Büsselberg, D., & Abdolghaffari, A. H. (2025) · Phytotherapy Research · doi:10.1002/ptr.8522 · Cited by 3
“Notably, TP53 mutations have been documented in nearly all types of cancer, with mutation rates ranging from 10%, as observed in hematopoietic malignancies, to almost 100%, as seen in high-grade serous ovarian carcinoma (Aylon and Oren 2011; Peller and Rotter 2003).”
Concurrent TP53 Mutation and Deletion in Refractory Low-grade Follicular Lymphoma
Khanlari, M., Wang, S. A., Fowler, N. H., Tang, G., Saluja, K., Muzzafar, T., Medeiros, L. J., & Thakral, B. (2021) · Clinical Lymphoma Myeloma & Leukemia · doi:10.1016/j.clml.2021.03.003 · Cited by 3
RETRACTED: UHRF2, another E3 ubiquitin ligase for p53
Bai, L., Wang, X., Jin, F., Yang, Y., Qian, G., & Duan, C. (2012) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2012.08.009 · Cited by 3
RetractedSun, Y., Myers, C. J., Dicker, A. P., & Lü, B. (2014) · PLoS ONE · doi:10.1371/journal.pone.0087492 · Cited by 3
“cellular stress, including DNA damage and hypoxia [15,46].”
BackgroundWasserman, J. K., AlGhamdi, D. A., de Almeida, J. R., Stockley, T. L., & Perez‐Ordoñez, B. (2018) · Head and Neck Pathology · doi:10.1007/s12105-018-0934-2 · Cited by 3
El-kott, A. F., ElBealy, E. R., Elsaid, F. G., El-Mekkawy, H. I., Abd-Lateif, A.-E.-K. M., Taweel, A., Khalifa, H. S., Kandeel, A. Y., Morsy, K., Ibrahim, E. H., et al. (2021) · Biocell · doi:10.32604/biocell.2021.012516 · Cited by 3
ANGEL2 Modulates Wild-type TP53 Translation and Doxorubicin Chemosensitivity in Colon Cancer
Lucchesi, C. A., Mantrala, S., Tran, D., Batra, N., Durve, A., Suen, C., Zhang, J., Ghosh, P., & Chen, X. (2025) · Molecular Cancer Research · doi:10.1158/1541-7786.mcr-24-0702 · Cited by 2
WITHDRAWN: MiR-200 family and cancer: Function, regulation and signaling
Chen, Y., & Zhang, L. (2014) · Surgical Oncology · doi:10.1016/j.suronc.2014.03.001 · Cited by 2
p53 as Batman: Using a Movie Plot to Understand Control of the Cell Cycle
Gadi, N., Foley, S. E., Nowey, M., & Plopper, G. E. (2013) · Science Signaling · doi:10.1126/scisignal.2003535 · Cited by 2
Rojas, M. L. (2011) · Digital Commons-TMC (Texas Medical Center) · Cited by 2
p53: Point Mutations, SNPs and Cancer
Fang, M., Simeonova, I., & Toledo, F. (2012) · InTech eBooks · doi:10.5772/33715 · Cited by 1
The Molecular Genetic Events in Colorectal Cancer and Diet
Naguib, A., Laura, J., Panagiota, N., & Mark, J. (2012) · InTech eBooks · doi:10.5772/29365
McEachin, R. C. (2011) · World Journal of Medical Genetics · doi:10.5496/wjmg.v1.i1.4
Regulation of Podosomes in Vascular Smooth Muscle Cell Invasion of the Extracellular Matrix
Mak, A. S. (2016) · WORLD SCIENTIFIC eBooks · doi:10.1142/9789813144064_0006
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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