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Article ; Online: p53: A tale of complexity and context.

Oren, Moshe / Prives, Carol

2024 Volume 187, Issue 7, Page(s) 1569–1573

Abstract: The story of p53 is illuminating. Despite widespread attention, the tumor-suppressive functions of wild-type p53 or the oncogenic activities of its cancer-associated mutants are still not fully understood, and our discoveries have not yet led to major ... ...

Abstract	The story of p53 is illuminating. Despite widespread attention, the tumor-suppressive functions of wild-type p53 or the oncogenic activities of its cancer-associated mutants are still not fully understood, and our discoveries have not yet led to major therapeutic breakthroughs. There is still much to learn about this fascinating protein.
MeSH term(s)	Humans ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Neoplasms/genetics ; Neoplasms/drug therapy ; Mutation
Chemical Substances	Tumor Suppressor Protein p53
Language	English
Publishing date	2024-03-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2024.02.043
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Zs.MG 58: Show issues

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Book ; Online: Transcriptional Regulation in Cancers and Metabolic Diseases

Prives, Carol / Zhou, Wen

2015

Abstract: The transcription factor (TF) mediated regulation of gene expression is a process fundamental to all biological and physiological processes. Genetic changes and epigenetic modifications of TFs affect target gene expression during the formation of ... ...

Abstract	The transcription factor (TF) mediated regulation of gene expression is a process fundamental to all biological and physiological processes. Genetic changes and epigenetic modifications of TFs affect target gene expression during the formation of malignant cells. Extensive work has been done on the critical TFs in various disease models. Despite the success of numerous TF-targeted therapies, there remain significant hurdles understanding the mechanisms, transcriptional targets and networks of physiologic pathways that govern TF action. This effort is now beginning to produce exciting new avenues of research. A clinically relevant topic for genetic change of TF is the mutant isoforms of p53, the most famous tumor suppressor. The p53 mutations either results in loss of function, or acting as dominant negative for wild-type protein, or 'gain of function' specifically promoting cancer survival.- The gain of function is achieved by shifting p53 binding partner proteins, or changed genomic binding landscape leading to a cancer-promoting transcriptome. Another example of genetic change of TF causing malignancy is the AML-ETO fusion protein in the human t(8;21)-leukemia. The fusion protein is an active TF, and more interestingly, new studies link the disease causing role of AML-ETO to the unique transcriptome in the hematopoietic stem cells. Nuclear receptors (NR) are a group of ligand-dependent TFs governing the expression of genes involved in a broad range of reproductive, developmental and metabolic programs. Genetic changes and epigenetic modifications of NRs lead to cancers and metabolic diseases. Androgen receptor (AR), estrogen receptor (ER) and progesterone receptor (PR) are well studied NRs in prostate, breast and endometrial cancers.- The development in sequencing technology and computational genomics enable us to investigate the transcription programs of these master TFs in an unprecedented level. This Research Topic aims to present the most up-to-date progress in the field of transcription regulation in cancers and metabolic diseases
Keywords	Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; Medicine (General) ; Diseases of the endocrine glands. Clinical endocrinology
Size	1 electronic resource (98 p.)
Publisher	Frontiers Media SA
Document type	Book ; Online
Note	English ; Open Access
HBZ-ID	HT020091141
ISBN	9782889197125 ; 2889197123
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Article ; Online: GLS2 shapes ferroptosis in hepatocellular carcinoma.

Suzuki, Sawako / Venkatesh, Divya / Tanaka, Tomoaki / Prives, Carol

Oncotarget

2023 Volume 14, Page(s) 900–903

MeSH term(s)	Humans ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/pathology ; Liver Neoplasms/genetics ; Liver Neoplasms/pathology ; Ferroptosis ; Tumor Suppressor Protein p53 ; Cell Line, Tumor ; Glutaminase/metabolism
Chemical Substances	Tumor Suppressor Protein p53 ; GLS2 protein, human (EC 3.5.1.2) ; Glutaminase (EC 3.5.1.2)
Language	English
Publishing date	2023-10-19
Publishing country	United States
Document type	Editorial
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.28526
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Article ; Online: O-GlcNAc transferase regulates p21 protein levels and cell proliferation through the FoxM1-Skp2 axis in a p53-independent manner.

de Queiroz, Rafaela Muniz / Moon, Sung-Hwan / Prives, Carol

The Journal of biological chemistry

2022 Volume 298, Issue 9, Page(s) 102289

Abstract: The protein product of the CDKN1A gene, p21, has been extensively characterized as a negative regulator of the cell cycle. Nevertheless, it is clear that p21 has manifold complex and context-dependent roles that can be either tumor suppressive or ... ...

Abstract	The protein product of the CDKN1A gene, p21, has been extensively characterized as a negative regulator of the cell cycle. Nevertheless, it is clear that p21 has manifold complex and context-dependent roles that can be either tumor suppressive or oncogenic. Most well studied as a transcriptional target of the p53 tumor suppressor protein, there are other means by which p21 levels can be regulated. In this study, we show that pharmacological inhibition or siRNA-mediated reduction of O-GlcNAc transferase (OGT), the enzyme responsible for glycosylation of intracellular proteins, increases expression of p21 in both p53-dependent and p53-independent manners in nontransformed and cancer cells. In cells harboring WT p53, we demonstrate that inhibition of OGT leads to p53-mediated transactivation of CDKN1A, while in cells that do not express p53, inhibiting OGT leads to increased p21 protein stabilization. p21 is normally degraded by the ubiquitin-proteasome system following ubiquitination by, among others, the E3 ligase Skp-Cullin-F-box complex; however, in this case, we show that blocking OGT causes impairment of the Skp-Cullin-F-box ubiquitin complex as a result of disruption of the FoxM1 transcription factor-mediated induction of Skp2 expression. In either setting, we conclude that p21 levels induced by OGT inhibition correlate with cell cycle arrest and decreased cancer cell proliferation.
MeSH term(s)	Cell Line, Tumor ; Cell Proliferation/physiology ; Cullin Proteins/metabolism ; Cyclin-Dependent Kinase Inhibitor p21/genetics ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; Forkhead Box Protein M1/metabolism ; Humans ; N-Acetylglucosaminyltransferases/antagonists & inhibitors ; N-Acetylglucosaminyltransferases/genetics ; N-Acetylglucosaminyltransferases/metabolism ; Proteasome Endopeptidase Complex/genetics ; Proteasome Endopeptidase Complex/metabolism ; Protein Stability ; RNA, Small Interfering ; S-Phase Kinase-Associated Proteins/metabolism ; Transcription Factors/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Ubiquitin/metabolism
Chemical Substances	CDKN1A protein, human ; Cullin Proteins ; Cyclin-Dependent Kinase Inhibitor p21 ; FOXM1 protein, human ; Forkhead Box Protein M1 ; RNA, Small Interfering ; S-Phase Kinase-Associated Proteins ; SKP2 protein, human ; TP53 protein, human ; Transcription Factors ; Tumor Suppressor Protein p53 ; Ubiquitin ; N-Acetylglucosaminyltransferases (EC 2.4.1.-) ; OGT protein, human (EC 2.4.1.255) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
Language	English
Publishing date	2022-07-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2022.102289
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Article ; Online: Discovering Transcription Factor Noncoding RNA Targets Using ChIP-Seq Analysis.

Fomin, Vitalay / Prives, Carol

Methods in molecular biology (Clifton, N.J.)

2020 Volume 2108, Page(s) 305–312

Abstract: Next generation sequencing enables large-scale analysis of mRNA expression (RNA-seq), genome variance (whole genome or exome), and transcription factor binding (ChIP-seq). Here we describe a method that allows the identification of transcription factor- ... ...

Abstract	Next generation sequencing enables large-scale analysis of mRNA expression (RNA-seq), genome variance (whole genome or exome), and transcription factor binding (ChIP-seq). Here we describe a method that allows the identification of transcription factor-binding sites in the vicinity of nonprotein-coding genes.
MeSH term(s)	Chromatin Immunoprecipitation Sequencing ; Computational Biology/methods ; Databases, Genetic ; Gene Expression Regulation ; High-Throughput Nucleotide Sequencing ; RNA, Untranslated/genetics ; Sequence Analysis, DNA ; Software ; Transcription Factors/genetics ; Web Browser
Chemical Substances	RNA, Untranslated ; Transcription Factors
Language	English
Publishing date	2020-01-14
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-0247-8_26
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Article ; Online: Gain-of-function mutant p53: history and speculation.

Bargonetti, Jill / Prives, Carol

Journal of molecular cell biology

2019 Volume 11, Issue 7, Page(s) 605–609

MeSH term(s)	Animals ; Gain of Function Mutation ; History, 20th Century ; History, 21st Century ; Humans ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/history ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	TP53 protein, human ; Tumor Suppressor Protein p53
Language	English
Publishing date	2019-07-05
Publishing country	United States
Document type	Historical Article ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2500949-7
ISSN	1759-4685 ; 1674-2788
ISSN (online)	1759-4685
ISSN	1674-2788
DOI	10.1093/jmcb/mjz067
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Article ; Online: A Non-Canonical Hippo Pathway Represses the Expression of ΔNp63.

Low-Calle, Ana Maria / Ghoneima, Hana / Ortega, Nicholas / Cuibus, Adriana M / Katz, Chen / Prives, Carol / Prywes, Ron

Molecular and cellular biology

2024 Volume 44, Issue 1, Page(s) 27–42

Abstract: The p63 transcription factor, a member of the p53 family, plays an oncogenic role in squamous cell carcinomas, while in breast cancers its expression is often repressed. In the canonical conserved Hippo pathway, known to play a complex role in regulating ...

Abstract	The p63 transcription factor, a member of the p53 family, plays an oncogenic role in squamous cell carcinomas, while in breast cancers its expression is often repressed. In the canonical conserved Hippo pathway, known to play a complex role in regulating growth of cancer cells, protein kinases MST1/2 and LATS1/2 act sequentially to phosphorylate and inhibit the YAP/TAZ transcription factors. We found that in MCF10A mammary epithelial cells as well as in squamous and breast cancer cell lines, expression of ΔNp63 RNA and protein is strongly repressed by inhibition of the Hippo pathway protein kinases. While MST1/2 and LATS1 are required for p63 expression, the next step of the pathway, namely phosphorylation and degradation of the YAP/TAZ transcriptional activators is not required for p63 repression. This suggests that regulation of p63 expression occurs by a noncanonical version of the Hippo pathway. We identified similarly regulated genes, suggesting the broader importance of this pathway. Interestingly, lowering p63 expression lead to increased YAP protein levels, indicating crosstalk of the YAP/TAZ-independent and -dependent branches of the Hippo pathway. These results, which reveal the intersection of the Hippo and p63 pathways, may prove useful for the control of their activities in cancer cells.
MeSH term(s)	Humans ; Hippo Signaling Pathway ; Signal Transduction ; Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; YAP-Signaling Proteins ; Protein Serine-Threonine Kinases/metabolism ; Transcription Factors/metabolism ; Phosphoproteins/genetics ; Phosphoproteins/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; YAP-Signaling Proteins ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Transcription Factors ; Phosphoproteins
Language	English
Publishing date	2024-01-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	779397-2
ISSN	1098-5549 ; 0270-7306
ISSN (online)	1098-5549
ISSN	0270-7306
DOI	10.1080/10985549.2023.2292037
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Article ; Online: Systematic characterization of p53-regulated long non-coding RNAs across human cancers reveals remarkable heterogeneity among different tumor types.

Regunath, Kausik / Fomin, Vitalay / Wang, Pingzhang / Liu, Zhaoqi / Hoque, Mainul / Tian, Bin / Rabadan, Raul / Prives, Carol

Molecular cancer research : MCR

2024

Abstract: The p53 tumor suppressor protein, a sequence specific DNA binding transcription factor, regulates the expression of a large number of genes, in response to various forms of cellular stress. While the protein coding target genes of p53 have been well ... ...

Abstract	The p53 tumor suppressor protein, a sequence specific DNA binding transcription factor, regulates the expression of a large number of genes, in response to various forms of cellular stress. While the protein coding target genes of p53 have been well studied, less is known about its role in regulating long non-coding genes and their functional relevance to cancer. Here we report the genome-wide identification of a large set (>1000) of long non-coding RNAs(lncRNAs) that are putative p53 targets in a colon cancer cell line and in human patient datasets from five different common types of cancer. These lncRNAs have not been annotated by other studies of normal unstressed systems. In the colon cancer cell line a high proportion of these lncRNAs are uniquely induced by different chemotherapeutic agents that activate p53, while others are induced by more than one agent tested. Further, subsets of these lncRNAs independently predict overall and disease-free survival of patients across the five different common cancer types. Interestingly, both genetic alterations and patient survival associated with different lncRNAs are unique to each cancer tested, indicating extraordinary tissue-specific variability in the p53 non-coding response. The newly identified non-coding p53 target genes have allowed us to construct a classifier for tumor diagnosis and prognosis. Implications: Our results not only identify myriad p53-regulated lncRNAs, they also reveal marked drug-induced, as well as tissue- and tumor-specific heterogeneity in these putative p53 targets and our findings have enabled the construction of robust classifiers for diagnosis and prognosis.
Language	English
Publishing date	2024-02-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-23-0295
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Article ; Online: p21 can be a barrier to ferroptosis independent of p53.

Venkatesh, Divya / Stockwell, Brent R / Prives, Carol

Aging

2020 Volume 12, Issue 18, Page(s) 17800–17814

Abstract: Traditionally, the p21 protein has been viewed as limiting cancer progression and promoting aging. In contrast, there are reports that p21 can enhance cancer survival and limit tissue damage, depending on the tissue of origin and type of stressor ... ...

Abstract	Traditionally, the p21 protein has been viewed as limiting cancer progression and promoting aging. In contrast, there are reports that p21 can enhance cancer survival and limit tissue damage, depending on the tissue of origin and type of stressor involved. Here, we provide evidence to support these latter two roles of p21 by exploring its ability to regulate ferroptosis. Ferroptosis is a form of cell death that is associated with certain degenerative diseases, some of which are aging-related. Our results reveal a correlation between p21 protein levels in cell lines that are resistant to ferroptosis (p21 high) versus cell lines that are sensitive and easily undergo ferroptosis (p21 low). We also show that p21 levels themselves are differentially regulated in response to ferroptosis in a p53-independent manner. Further, experimentally altering the abundance of p21 protein inverts the ferroptosis-sensitivity of both resistant and sensitive human cancer cell lines. Our data also indicate that the interaction of p21 with CDKs is crucial for its ability to restrict the progression of ferroptosis. While this study was performed in cancer cell lines, our results support the potential of p21 to aid in maintenance of healthy tissues by blocking the damage incurred due to ferroptosis.
Language	English
Publishing date	2020-09-24
Publishing country	United States
Document type	Journal Article
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.103961
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Article ; Online: The roles and regulation of MDM2 and MDMX: it is not just about p53.

Klein, Alyssa M / de Queiroz, Rafaela Muniz / Venkatesh, Divya / Prives, Carol

Genes & development

2021 Volume 35, Issue 9-10, Page(s) 575–601

Abstract: Most well studied as proteins that restrain the p53 tumor suppressor protein, MDM2 and MDMX have rich lives outside of their relationship to p53. There is much to learn about how these two proteins are regulated and how they can function in cells that ... ...

Abstract	Most well studied as proteins that restrain the p53 tumor suppressor protein, MDM2 and MDMX have rich lives outside of their relationship to p53. There is much to learn about how these two proteins are regulated and how they can function in cells that lack p53. Regulation of MDM2 and MDMX, which takes place at the level of transcription, post-transcription, and protein modification, can be very intricate and is context-dependent. Equally complex are the myriad roles that these two proteins play in cells that lack wild-type p53; while many of these independent outcomes are consistent with oncogenic transformation, in some settings their functions could also be tumor suppressive. Since numerous small molecules that affect MDM2 and MDMX have been developed for therapeutic outcomes, most if not all designed to prevent their restraint of p53, it will be essential to understand how these diverse molecules might affect the p53-independent activities of MDM2 and MDMX.
MeSH term(s)	Animals ; Gene Expression Regulation, Neoplastic ; Humans ; Promoter Regions, Genetic/genetics ; Proto-Oncogene Proteins c-mdm2/genetics ; Proto-Oncogene Proteins c-mdm2/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Transcription Factors ; Tumor Suppressor Protein p53 ; Proto-Oncogene Proteins c-mdm2 (EC 2.3.2.27)
Language	English
Publishing date	2021-04-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	806684-x
ISSN	1549-5477 ; 0890-9369
ISSN (online)	1549-5477
ISSN	0890-9369
DOI	10.1101/gad.347872.120
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Zs.MG 54: Show issues

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