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9.9
5.1
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Cells
Special Issues
p53 Signaling and Cancer
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p53 Signaling and Cancer

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

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 8933

Special Issue Editors

Dr. Yasumichi Inoue

E-Mail Website
Guest Editor
Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan
Interests: cancer; cell cycle; cellular senescence; endoplasmic reticulum stress; molecular target drugs; p53; transcriptional regulation
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Hidetoshi Hayashi

E-Mail Website1 Website2
Guest Editor
Department of Cell Signaling, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya 467-8603, Japan
Interests: cancer; cell cycle; cellular senescence; endoplasmic reticulum stress; molecular target drugs; p53; transcriptional regulation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

About 40 years ago, p53 was initially discovered as a protein that binds to the large T antigen of the tumor virus SV40. However, since the p53 was proven to be a tumor suppressor in 1989, research on p53 has always attracted researchers from all over the world through the use of advanced technologies. However, despite more than 40 years of research, p53-regulated tumor suppression mechanisms remain a mystery, with the induction of cell death and cell cycle arrest considered to be among the most relevant regulatory aspects. In addition to cell death by apoptosis induction by p53, the mechanism of tumor suppressive effect of p53 has been broadened to include ferroptosis regulation by iron-dependent lipid peroxidation. Furthermore, recent studies are revealing that p53 exerts its tumor suppressive effects by regulating energy metabolism, antioxidant function, and metabolic reprogramming in cells. Thus, it is still necessary to elucidate the ever-expanding tumor suppressive function of p53. Here, we welcome original papers and review articles that will help us to understand the tumor suppressor role of p53 in cancer. In addition, papers on the study of p53 signaling and the development of therapies will be discussed.

Dr. Yasumichi Inoue
Prof. Dr. Hidetoshi Hayashi
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
  • apoptosis
  • cell cycle
  • ferroptosis
  • cancer therapy
  • signal transduction

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Published Papers (3 papers)

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Research

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14 pages, 4502 KiB  
Article
Inhibiting WEE1 Augments the Antitumor Efficacy of Cisplatin in Urothelial Carcinoma by Enhancing the DNA Damage Process
by Yu-Li Su, Ling-Yi Xiao, Shih-Yu Huang, Chia-Che Wu, Li-Chung Chang, Yi-Hua Chen, Hao-Lun Luo, Chun-Chieh Huang, Ting-Ting Liu and Jei-Ming Peng
Cells 2023, 12(11), 1471; https://doi.org/10.3390/cells12111471 - 25 May 2023
Cited by 3 | Viewed by 2128
Abstract
Urothelial carcinoma (UC) is characterized by a high incidence of TP53 mutation, and overcoming resistance to cisplatin-based chemotherapy in UC is a major concern. Wee1 is a G2/M phase regulator that controls the DNA damage response to chemotherapy in TP53-mutant cancers. The [...] Read more.
Urothelial carcinoma (UC) is characterized by a high incidence of TP53 mutation, and overcoming resistance to cisplatin-based chemotherapy in UC is a major concern. Wee1 is a G2/M phase regulator that controls the DNA damage response to chemotherapy in TP53-mutant cancers. The combination of Wee1 blockade with cisplatin has shown synergistic efficacy in several types of cancers, but little is known regarding UC. The antitumor efficacy of the Wee1 inhibitor (AZD-1775) alone or in combination with cisplatin was evaluated in UC cell lines and a xenograft mouse model. AZD-1775 enhanced the anticancer activity of cisplatin by increasing cellular apoptosis. AZD-1775 inhibited the G2/M checkpoint, improving the sensitivity of mutant TP53 UC cells to cisplatin by enhancing the DNA damage process. We confirmed that AZD-1775 combined with cisplatin reduced tumor volume and proliferation activity and increased the markers of cell apoptosis and DNA damage in the mouse xenograft model. In summary, the Wee1 inhibitor AZD-1775 combined with cisplatin elicited a promising anticancer efficacy in UC, and constitutes an innovative and promising therapeutic strategy. Full article
(This article belongs to the Special Issue p53 Signaling and Cancer)
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Review

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19 pages, 1101 KiB  
Review
Encoding and Decoding of p53 Dynamics in Cellular Response to Stresses
by Ping Wang, Hang-Yu Wang, Xing-Jie Gao, Hua-Xia Zhu, Xiao-Peng Zhang, Feng Liu and Wei Wang
Cells 2023, 12(3), 490; https://doi.org/10.3390/cells12030490 - 2 Feb 2023
Cited by 7 | Viewed by 2648
Abstract
In the cellular response to stresses, the tumor suppressor p53 is activated to maintain genomic integrity and fidelity. As a transcription factor, p53 exhibits rich dynamics to allow for discrimination of the type and intensity of stresses and to direct the selective activation [...] Read more.
In the cellular response to stresses, the tumor suppressor p53 is activated to maintain genomic integrity and fidelity. As a transcription factor, p53 exhibits rich dynamics to allow for discrimination of the type and intensity of stresses and to direct the selective activation of target genes involved in different processes including cell cycle arrest and apoptosis. In this review, we focused on how stresses are encoded into p53 dynamics and how the dynamics are decoded into cellular outcomes. Theoretical modeling may provide a global view of signaling in the p53 network by coupling the encoding and decoding processes. We discussed the significance of modeling in revealing the mechanisms of the transition between p53 dynamic modes. Moreover, we shed light on the crosstalk between the p53 network and other signaling networks. This review may advance the understanding of operating principles of the p53 signaling network comprehensively and provide insights into p53 dynamics-based cancer therapy. Full article
(This article belongs to the Special Issue p53 Signaling and Cancer)
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21 pages, 1536 KiB  
Review
Insights into Regulators of p53 Acetylation
by Mai Nagasaka, Chiharu Miyajima, Hiromasa Aoki, Mineyoshi Aoyama, Daisuke Morishita, Yasumichi Inoue and Hidetoshi Hayashi
Cells 2022, 11(23), 3825; https://doi.org/10.3390/cells11233825 - 29 Nov 2022
Cited by 16 | Viewed by 3428
Abstract
The tumor suppressor p53 is a transcription factor that regulates the expression of dozens of target genes and diverse physiological processes. To precisely regulate the p53 network, p53 undergoes various post-translational modifications and alters the selectivity of target genes. Acetylation plays an essential [...] Read more.
The tumor suppressor p53 is a transcription factor that regulates the expression of dozens of target genes and diverse physiological processes. To precisely regulate the p53 network, p53 undergoes various post-translational modifications and alters the selectivity of target genes. Acetylation plays an essential role in cell fate determination through the activation of p53. Although the acetylation of p53 has been examined, the underlying regulatory mechanisms remain unclear and, thus, have attracted the interest of researchers. We herein discuss the role of acetylation in the p53 pathway, with a focus on p53 acetyltransferases and deacetylases. We also review recent findings on the regulators of these enzymes to understand the mode of p53 acetylation from a broader perspective. Full article
(This article belongs to the Special Issue p53 Signaling and Cancer)
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