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Biomolecules
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Advances in p53 Research 2024
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Advances in p53 Research 2024

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 31 December 2024 | Viewed by 2340

Special Issue Editor

Dr. Gabriella D’Orazi

E-Mail Website
Guest Editor
1. Department of Neuroscience and Imaging, University G. D’Annunzio, 66013 Chieti, Italy
2. Department of Research, Unit of Cellular Network and Therapeutic Innovation, Regina Elena National Cancer Institute, 00144 Rome, Italy
Interests: tumor biology; molecular oncology; onco-suppressor p53; autophagy; hypoxia; oxidative stress; tumor microenvironment; glioblastoma; personalized medicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue concerns p53, one of the most intensively studied tumor suppressor proteins that, in some circumstances, can acquire oncogenic function. Since its discovery, many cellular functions have been ascribed to p53, such as transcription regulation and signalling to apoptosis, involvement in the response to stress, senescence, DNA repair, metabolism, immunity, and epigenetic regulation. The perturbation of p53 signalling pathways is required for the development of most cancers, and studies regarding the restoration or reactivation of p53 function have recently showed significant therapeutic benefit. Over half of all human cancers demonstrate alterations in p53 that not only attenuate or eliminate its tumor suppressor function, but can also result in the gain of a novel transforming function, thus contributing to cancer progression. Much knowledge still needs to be acquired regarding the multiple facets of this intriguing protein. Here, we welcome papers describing recent advances in understanding p53 function and dysfunction, with an emphasis on novel molecules which target p53 reactivation for translational purposes.

Dr. Gabriella D’Orazi
Guest Editor

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. Biomolecules is an international peer-reviewed open access monthly 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
  • small molecules
  • tumor suppressor
  • apoptosis
  • tumor–host interaction
  • targeted therapies
  • tumor microenvironment (TME)

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Related Special Issue

Published Papers (2 papers)

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19 pages, 6051 KiB  
Article
Hepatitis B Virus X Protein Induces Reactive Oxygen Species Generation via Activation of p53 in Human Hepatoma Cells
by Seungyeon Kim, Jimin Park, Jiwoo Han and Kyung Lib Jang
Biomolecules 2024, 14(10), 1201; https://doi.org/10.3390/biom14101201 - 24 Sep 2024
Viewed by 557
Abstract
Hepatitis B virus (HBV), particularly through the HBx protein, induces oxidative stress during liver infections. This study reveals that HBx increases reactive oxygen species (ROS) via two distinct mechanisms. The first mechanism is p53-independent, likely involving mitochondrial dysfunction, as demonstrated by elevated ROS [...] Read more.
Hepatitis B virus (HBV), particularly through the HBx protein, induces oxidative stress during liver infections. This study reveals that HBx increases reactive oxygen species (ROS) via two distinct mechanisms. The first mechanism is p53-independent, likely involving mitochondrial dysfunction, as demonstrated by elevated ROS levels in p53-deficient Hep3B cells and p53-knocked-down HepG2 cells after HBx expression or HBV infection. The increase in ROS persisted even when p53 transcriptional activity was inhibited by pifithrin-α (PFT-α), a p53 inhibitor. The second mechanism is p53-dependent, wherein HBx activates p53, which then amplifies ROS production through a feedback loop involving ROS and p53. The ability of HBx to elevate ROS levels was higher in HepG2 than in Hep3B cells. Knocking down p53 in HepG2 cells lowered ROS levels, while ectopic p53 expression in Hep3B cells raised ROS. HBx-activated p53 downregulated catalase and upregulated manganese-dependent superoxide dismutase, contributing to ROS amplification. The transcriptional activity of p53 was crucial for these effects, as cells with a p53 R175H mutation or those treated with PFT-α generated less ROS. Additionally, HBx variants with Ser-101 increased p53 and ROS levels, whereas variants with Pro-101 did not. These dual mechanisms of HBx-induced ROS generation are likely significant in the pathogenesis of HBV and may contribute to liver diseases, including hepatocellular carcinoma. Full article
(This article belongs to the Special Issue Advances in p53 Research 2024)
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Review

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24 pages, 2918 KiB  
Review
Recent Advances on Mutant p53: Unveiling Novel Oncogenic Roles, Degradation Pathways, and Therapeutic Interventions
by Marco Cordani, Alessia Garufi, Rossella Benedetti, Marco Tafani, Michele Aventaggiato, Gabriella D’Orazi and Mara Cirone
Biomolecules 2024, 14(6), 649; https://doi.org/10.3390/biom14060649 - 31 May 2024
Viewed by 1358
Abstract
The p53 protein is the master regulator of cellular integrity, primarily due to its tumor-suppressing functions. Approximately half of all human cancers carry mutations in the TP53 gene, which not only abrogate the tumor-suppressive functions but also confer p53 mutant proteins with oncogenic [...] Read more.
The p53 protein is the master regulator of cellular integrity, primarily due to its tumor-suppressing functions. Approximately half of all human cancers carry mutations in the TP53 gene, which not only abrogate the tumor-suppressive functions but also confer p53 mutant proteins with oncogenic potential. The latter is achieved through so-called gain-of-function (GOF) mutations that promote cancer progression, metastasis, and therapy resistance by deregulating transcriptional networks, signaling pathways, metabolism, immune surveillance, and cellular compositions of the microenvironment. Despite recent progress in understanding the complexity of mutp53 in neoplastic development, the exact mechanisms of how mutp53 contributes to cancer development and how they escape proteasomal and lysosomal degradation remain only partially understood. In this review, we address recent findings in the field of oncogenic functions of mutp53 specifically regarding, but not limited to, its implications in metabolic pathways, the secretome of cancer cells, the cancer microenvironment, and the regulating scenarios of the aberrant proteasomal degradation. By analyzing proteasomal and lysosomal protein degradation, as well as its connection with autophagy, we propose new therapeutical approaches that aim to destabilize mutp53 proteins and deactivate its oncogenic functions, thereby providing a fundamental basis for further investigation and rational treatment approaches for TP53-mutated cancers. Full article
(This article belongs to the Special Issue Advances in p53 Research 2024)
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