Protein Kinases and Pseudokinases in Cancers

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: 1 May 2024 | Viewed by 1543

Special Issue Editors


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Guest Editor
1. Faculdade de Medicina e Ciências Biomédicas (FMCB), Campus de Gambelas, Universidade do Algarve, 8005-139 Faro, Portugal
2. Algarve Biomedical Center Research Institute, ABC-RI, 8005-139 Faro, Portugal
Interests: cancer signaling; drug resistance; genomic alterations; copy number variations
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
1. Algarve Biomedical Center Research Institute, ABC-RI, 8005-139 Faro, Portugal
2. Escola Superior de Saúde (ESSUAlg), Campus de Gambelas, Universidade do Algarve, 8005-139 Faro, Portugal
Interests: metabolism; cancer; metabolic reprogramming; Tribbles; drug repurposing; therapy resistance; cell signaling
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Protein kinases and pseudokinases are a superfamily of proteins and account for about 2% of human genes. This family of proteins mediates the activation of key signaling pathways involved in many biological processes. Hence, mutations affecting these groups of proteins are known to be associated with human tumor onset and progression. So far, more than 70 small molecule inhibitors have been approved by the FDA, poising kinases as the second most important targets of precision therapy. However, development of drug resistance is still a major hurdle to overcome. Therefore, understanding the fundamental molecular mechanisms by which kinases and pseudokinases modulate cancer development will severely impact the design of more effective inhibitors.

In this Special Issue of Cancers, we invite authors to submit contributions that provide novel findings in the field of kinases and pseudokinases. We will cover recent advances on the basic mechanisms by which kinases/pseudokinases modulate cancer development and mechanisms of drug resistance or development of new therapeutic approaches. We welcome results from the basic research, preclinical, or clinical fields. Reviews that highlight new findings in the areas mentioned above are also welcome.

We look forward to receiving your contributions.

Dr. Bibiana I. Ferreira
Dr. Ana Luísa De Sousa-Coelho
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. Cancers 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 2900 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

  • protein kinase
  • pseudokinase
  • cancer signaling
  • kinase inhibitor
  • cancer
  • targeted therapy
  • drug resistance

Published Papers (1 paper)

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Review

14 pages, 2171 KiB  
Review
The Important Role of Protein Kinases in the p53 Sestrin Signaling Pathway
by Karsten Gülow, Deniz Tümen and Claudia Kunst
Cancers 2023, 15(22), 5390; https://doi.org/10.3390/cancers15225390 - 13 Nov 2023
Viewed by 950
Abstract
p53, a crucial tumor suppressor and transcription factor, plays a central role in the maintenance of genomic stability and the orchestration of cellular responses such as apoptosis, cell cycle arrest, and DNA repair in the face of various stresses. Sestrins, a group of [...] Read more.
p53, a crucial tumor suppressor and transcription factor, plays a central role in the maintenance of genomic stability and the orchestration of cellular responses such as apoptosis, cell cycle arrest, and DNA repair in the face of various stresses. Sestrins, a group of evolutionarily conserved proteins, serve as pivotal mediators connecting p53 to kinase-regulated anti-stress responses, with Sestrin 2 being the most extensively studied member of this protein family. These responses involve the downregulation of cell proliferation, adaptation to shifts in nutrient availability, enhancement of antioxidant defenses, promotion of autophagy/mitophagy, and the clearing of misfolded proteins. Inhibition of the mTORC1 complex by Sestrins reduces cellular proliferation, while Sestrin-dependent activation of AMP-activated kinase (AMPK) and mTORC2 supports metabolic adaptation. Furthermore, Sestrin-induced AMPK and Unc-51-like protein kinase 1 (ULK1) activation regulates autophagy/mitophagy, facilitating the removal of damaged organelles. Moreover, AMPK and ULK1 are involved in adaptation to changing metabolic conditions. ULK1 stabilizes nuclear factor erythroid 2-related factor 2 (Nrf2), thereby activating antioxidative defenses. An understanding of the intricate network involving p53, Sestrins, and kinases holds significant potential for targeted therapeutic interventions, particularly in pathologies like cancer, where the regulatory pathways governed by p53 are often disrupted. Full article
(This article belongs to the Special Issue Protein Kinases and Pseudokinases in Cancers)
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