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9.9
5.1
Journals
Cells
Special Issues
p53 Regulation Mechanisms
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p53 Regulation Mechanisms

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 26233

Special Issue Editors

Prof. Dr. Ji Hoon Jung

E-Mail Website
Guest Editor
Department of Science in Korean Medicine, Graduate School, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Republic of Korea
Interests: ferroptosis; p53; cancer metabolism; natural compound
Special Issues, Collections and Topics in MDPI journals
Dr. Peng Liao

E-Mail Website
Co-Guest Editor
Surgery Department, University of Michigan, Ann Arbor, MI, USA
Interests: p53 mutations; p53–MDM2 feedback roop; regulation of c-Myc; c-Myc protein stability; histone modifications; immune response; EMT
Dr. Hyemin Lee

E-Mail Website
Co-Guest Editor
Tulane University, New Orleans, LA, USA
Interests: p53–MDM2 feedback roop; regulation of c-Myc; liver cancer; cancer biology; melatonin; natural compounds; cancer stem cells

Special Issue Information

Dear Colleagues,

The tumor suppressor p53 is frequently mutated in various human cancers as it can prevent tumorigenesis by inducing cellular senescence, regulating energy metabolism, blocking metastasis, stopping cell proliferation, and inducing apoptosis, mainly via its transcriptional activity. In response to various stressors, p53 is activated to induce or repress the transcription of numerous target genes important for multiple biological functions. For example, the p53 target gene p21 is involved in p53-dependent cell cycle arrest, while the BH3-only-encoding target genes BBC3 (Puma) and PMAIP1 (Noxa) play key roles in p53-mediated apoptosis. Since activated p53 is generally cytotoxic, it is subjected to tight regulation by MDM2, which is encoded by a transcriptional target gene of p53. Via its N-terminal domain, MDM2 directly binds to the N and C termini of p53 and mediates its ubiquitin-dependent proteolysis, as it possesses intrinsic E3 ubiquitin ligase activity, thus creating a negative feedback loop. The main focus of this Special Issue will be on the broad spectrum of functions of p53 in cancer cells.

We invite all scientists working on p53 to participate in this Special Issue. Original research articles or reviews on all aspects of the molecular and cellular mechanisms modulated by p53 in cancer cells are welcome.

We look forward to your contributions.

Dr. Ji Hoon Jung
Dr. Peng Liao
Dr. Hyemin Lee
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • p53
  • tumor suppressor
  • p53 target gene
  • MDM2
  • novel gene
  • cancer therapy

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Published Papers (6 papers)

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Research

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11 pages, 1851 KiB  
Article
Improvement of Cell Growth of Uterosacral Ligament Fibroblast Derived from Pelvic Organ Prolapse Patients by Cold Atmospheric Plasma Treated Liquid
by Ihn Han, Seung Ah Choi, Seul I Kim, Eun Ha Choi, Young Joo Lee and Youngsun Kim
Cells 2021, 10(10), 2728; https://doi.org/10.3390/cells10102728 - 13 Oct 2021
Cited by 4 | Viewed by 2964
Abstract
Pelvic organ prolapse (POP) is a chronic disorder that affects quality of life in women. Several POP treatments may be accompanied by abrasion, constant infection, and severe pain. Therefore, new treatment methods and improvements in current treatments for POP are required. Non-thermal atmospheric-pressure [...] Read more.
Pelvic organ prolapse (POP) is a chronic disorder that affects quality of life in women. Several POP treatments may be accompanied by abrasion, constant infection, and severe pain. Therefore, new treatment methods and improvements in current treatments for POP are required. Non-thermal atmospheric-pressure plasma is a rising biomedical therapy that generates a mixed cocktail of reactive species by different mechanisms. In this study, we applied a cylinder-type dielectric barrier discharge plasma device to create a plasma-treated liquid (PTL). The PTL was added to primary cultured human uterosacral ligament fibroblast (hUSLF) cells from POP patients at each stage. Surprisingly, treatment with diluted PTL increased hUSLF cell viability but decreased ovarian cancer cell viability. PTL also decreased cell apoptosis in hUSLF cells but increased it in SKOV3 cells. Our results suggest that PTL protects hUSLF cells from cell apoptosis by controlling the p53 pathway and improves cell viability, implying that PTL is a promising application for POP therapy. Full article
(This article belongs to the Special Issue p53 Regulation Mechanisms)
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15 pages, 1698 KiB  
Article
The Impact of Chlorambucil and Valproic Acid on Cell Viability, Apoptosis and Expression of p21, HDM2, BCL2 and MCL1 Genes in Chronic Lymphocytic Leukemia
by Katarzyna Lipska, Agata Filip and Anna Gumieniczek
Cells 2021, 10(5), 1088; https://doi.org/10.3390/cells10051088 - 2 May 2021
Cited by 3 | Viewed by 2290
Abstract
Malignant cells in chronic lymphocytic leukemia (CLL) show resistance to apoptosis, as well as to chemotherapy, which are related to deletions or mutations of TP53, high expression of MCL1 and BCL2 genes and other abnormalities. Thus, the main goal of the present [...] Read more.
Malignant cells in chronic lymphocytic leukemia (CLL) show resistance to apoptosis, as well as to chemotherapy, which are related to deletions or mutations of TP53, high expression of MCL1 and BCL2 genes and other abnormalities. Thus, the main goal of the present study was to assess the impact of chlorambucil (CLB) combined with valproic acid (VPA), a known antiepileptic drug and histone deacetylation inhibitor, on apoptosis of the cells isolated from 17 patients with CLL. After incubation with CLB (17.5 µM) and VPA (0.5 mM), percentage of apoptosis, as well as expression of two TP53 target genes (p21 and HDM2) and two genes from Bcl-2 family (BCL2 and MCL1), were tested. As a result, an increased percentage of apoptosis was observed for CLL cells treated with CLB and VPA, and with CLB alone. Under the treatment with the drug combination, the expression of p21 gene was visibly higher than under the treatment with CLB alone. At the same time, the cultures under CLB treatment showed visibly higher expression of BCL2 than the cultures with VPA alone. Thus, the present study strongly suggests further investigations on the CLB and VPA combination in CLL treatment. Full article
(This article belongs to the Special Issue p53 Regulation Mechanisms)
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13 pages, 3282 KiB  
Article
Non-Thermal Biocompatible Plasma Jet Induction of Apoptosis in Brain Cancer Cells
by Mahmuda Akter, Jun Sup Lim, Eun Ha Choi and Ihn Han
Cells 2021, 10(2), 236; https://doi.org/10.3390/cells10020236 - 26 Jan 2021
Cited by 16 | Viewed by 3483
Abstract
Glioblastoma multiforme (GBM) is a highly malignant and rapidly advancing astrocytic brain tumor in adults. Current therapy possibilities are chemotherapy, surgical resection, and radiation. The complexity of drug release through the blood-brain barrier, tumor reaction to chemotherapy, and the inherent resistance of tumor [...] Read more.
Glioblastoma multiforme (GBM) is a highly malignant and rapidly advancing astrocytic brain tumor in adults. Current therapy possibilities are chemotherapy, surgical resection, and radiation. The complexity of drug release through the blood-brain barrier, tumor reaction to chemotherapy, and the inherent resistance of tumor cells present challenges. New therapies are needed for individual use or combination with conventional methods for more effective treatment and improved survival for patients. GBM is difficult to treat because it grows quickly, spreads finger-shaped tentacles, and creates an irregular margin of normal tissue surrounding the tumor. Non-thermal biocompatible plasma (NBP) has recently been shown to selectively target cancer cells with minimal effects on regular cells, acting by generating reactive oxygen species (ROS) and reactive nitrogen species (RNS). We applied a soft jet plasma device with a syringe shape to U87 MG cells and astrocytes. Our results show that NBP-J significantly inhibits cell proliferation and changes morphology, induces cell cycle arrest, inhibits the survival pathway, and induces apoptosis. Our results indicate that NBP-J may be an efficient and safe clinical device for brain cancer therapy. Full article
(This article belongs to the Special Issue p53 Regulation Mechanisms)
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Review

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12 pages, 553 KiB  
Review
The Intricate Role of p53 in Adipocyte Differentiation and Function
by Yun Kyung Lee, Yu Seong Chung, Ji Hye Lee, Jin Mi Chun and Jun Hong Park
Cells 2020, 9(12), 2621; https://doi.org/10.3390/cells9122621 - 7 Dec 2020
Cited by 18 | Viewed by 4410
Abstract
For more than three decades, numerous studies have demonstrated the function of p53 in cell cycle, cellular senescence, autophagy, apoptosis, and metabolism. Among diverse functions, the essential role of p53 is to maintain cellular homeostatic response to stress by regulating proliferation and apoptosis. [...] Read more.
For more than three decades, numerous studies have demonstrated the function of p53 in cell cycle, cellular senescence, autophagy, apoptosis, and metabolism. Among diverse functions, the essential role of p53 is to maintain cellular homeostatic response to stress by regulating proliferation and apoptosis. Recently, adipocytes have been studied with increasing intensity owing to the increased prevalence of metabolic diseases posing a serious public health concern and because metabolic dysfunction can directly induce tumorigenesis. The prevalence of metabolic diseases has steadily increased worldwide, and a growing interest in these diseases has led to the focus on the role of p53 in metabolism and adipocyte differentiation with or without metabolic stress. However, our collective understanding of the direct role of p53 in adipocyte differentiation and function remains insufficient. Therefore, this review focuses on the newly discovered roles of p53 in adipocyte differentiation and function. Full article
(This article belongs to the Special Issue p53 Regulation Mechanisms)
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13 pages, 895 KiB  
Review
RBM10, a New Regulator of p53
by Ji Hoon Jung, Hyemin Lee, Shelya X Zeng and Hua Lu
Cells 2020, 9(9), 2107; https://doi.org/10.3390/cells9092107 - 16 Sep 2020
Cited by 21 | Viewed by 7606
Abstract
The tumor suppressor p53 acts as a transcription factor that regulates the expression of a number of genes responsible for DNA repair, cell cycle arrest, metabolism, cell migration, angiogenesis, ferroptosis, senescence, and apoptosis. It is the most commonly silenced or mutated gene in [...] Read more.
The tumor suppressor p53 acts as a transcription factor that regulates the expression of a number of genes responsible for DNA repair, cell cycle arrest, metabolism, cell migration, angiogenesis, ferroptosis, senescence, and apoptosis. It is the most commonly silenced or mutated gene in cancer, as approximately 50% of all types of human cancers harbor TP53 mutations. Activation of p53 is detrimental to normal cells, thus it is tightly regulated via multiple mechanisms. One of the recently identified regulators of p53 is RNA-binding motif protein 10 (RBM10). RBM10 is an RNA-binding protein frequently deleted or mutated in cancer cells. Its loss of function results in various deformities, such as cleft palate and malformation of the heart, and diseases such as lung adenocarcinoma. In addition, RBM10 mutations are frequently observed in lung adenocarcinomas, colorectal carcinomas, and pancreatic ductal adenocarcinomas. RBM10 plays a regulatory role in alternative splicing. Several recent studies not only linked this splicing regulation of RBM10 to cancer development, but also bridged RBM10′s anticancer function to the p53 pathway. This review will focus on the current progress in our understanding of RBM10 regulation of p53, and its role in p53-dependent cancer prevention. Full article
(This article belongs to the Special Issue p53 Regulation Mechanisms)
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16 pages, 512 KiB  
Review
The Janus Face of p53-Targeting Ubiquitin Ligases
by Qian Hao, Yajie Chen and Xiang Zhou
Cells 2020, 9(7), 1656; https://doi.org/10.3390/cells9071656 - 9 Jul 2020
Cited by 12 | Viewed by 4070
Abstract
The tumor suppressor p53 prevents tumorigenesis and cancer progression by maintaining genomic stability and inducing cell growth arrest and apoptosis. Because of the extremely detrimental nature of wild-type p53, cancer cells usually mutate the TP53 gene in favor of their survival and propagation. [...] Read more.
The tumor suppressor p53 prevents tumorigenesis and cancer progression by maintaining genomic stability and inducing cell growth arrest and apoptosis. Because of the extremely detrimental nature of wild-type p53, cancer cells usually mutate the TP53 gene in favor of their survival and propagation. Some of the mutant p53 proteins not only lose the wild-type activity, but also acquire oncogenic function, namely “gain-of-function”, to promote cancer development. Growing evidence has revealed that various E3 ubiquitin ligases are able to target both wild-type and mutant p53 for degradation or inactivation, and thus play divergent roles leading to cancer cell survival or death in the context of different p53 status. In this essay, we reviewed the recent progress in our understanding of the p53-targeting E3 ubiquitin ligases, and discussed the potential clinical implications of these E3 ubiquitin ligases in cancer therapy. Full article
(This article belongs to the Special Issue p53 Regulation Mechanisms)
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