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8.3
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Biomolecules
Special Issues
Kinases Signaling in Cancers
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Kinases Signaling in Cancers

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

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 12610

Special Issue Editors

Dr. Anastasia De Luca

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Guest Editor
Department of Biology, University of Rome Tor Vergata, Rome, Italy
Interests: breast cancer; epithelial to mesenchymal transition (EMT); metastasis; copper homeostasis in cancer; cuproproteins in cancer; glutathione-S-transferase; glutathionylation
Special Issues, Collections and Topics in MDPI journals
Dr. Luisa Rossi

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Guest Editor
Department of Biology, Tor Vergata University of Rome, Rome, Italy
Interests: copper; oxidative stress; mitochondria; neurodegeneration; proteins; biochemistry; enzymes
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Protein kinases are a large array of proteins which surveil signaling pathways and orchestrate fundamental physiological processes and cellular functions, such as development, hormone response and inflammation. They include: mitogen-activated protein kinases (MAPKs), triggered following stimulation at the cell surface of the tyrosine kinase receptors and G-coupled protein receptors; cyclin-dependent kinases (CDK), which respond to cyclins signaling; lipid kinases on plasma or organelle membranes (e.g. phosphoinositide 3-kinase, PI3K); autophagy-activated kinases (Unc-51, such as autophagy-activating kinase, ULK1/2), and Janus kinase–signal transducer and activator of transcription (JAK-STAT), which are a family of nonreceptor tyrosine kinases responding to intracellular cytokines. Their intracellular activity is regulated by different modulators (e.g., hormones, growth factors, cytokines and transition metals) which direct cells to their ultimate fate.

Upon dysregulation of their function, they are engaged in cancer initiation and progression and also in the acquisition of drug resistance. Thus, kinases have been the subject of intense research to unveil the underlying mechanisms and also as drug targets for cancer, particularly focusing on the identification of inhibitors to be used for clinical use.

This Special Issue aims to collect the most recent work in this field, in order to prompt further research, to pinpoint novel mechanisms underlying kinases involvement in cancer, and to suggest possible kinase-targeted drugs applicable in therapy.

Dr. Anastasia De Luca
Dr. Luisa Rossi
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. 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

  • kinases
  • cancer progression
  • signaling cascade
  • cancer progression
  • drug resistance

Published Papers (3 papers)

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Review

14 pages, 2008 KiB  
Review
Kinase Signaling in Colitis-Associated Colon Cancer and Inflammatory Bowel Disease
by Michelle Temby, Theresa L. Boye, Jacqueline Hoang, Ole H. Nielsen and John Gubatan
Biomolecules 2023, 13(11), 1620; https://0-doi-org.brum.beds.ac.uk/10.3390/biom13111620 - 6 Nov 2023
Cited by 1 | Viewed by 1748
Abstract
Colorectal cancer is a known complication of chronic inflammation of the colon (“colitis-associated colon cancer”). Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract. Patients with IBD are at increased risk of colon cancer compared to the general population. [...] Read more.
Colorectal cancer is a known complication of chronic inflammation of the colon (“colitis-associated colon cancer”). Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract. Patients with IBD are at increased risk of colon cancer compared to the general population. Kinase signaling pathways play critical roles in both the inflammation and regulating cellular processes such as proliferation and survival that contribute to cancer development. Here we review the interplay of kinase signaling pathways (mitogen-activated protein kinases, cyclin-dependent kinases, autophagy-activated kinases, JAK-STAT, and other kinases) and their effects on colitis-associated colon cancer. We also discuss the role of JAK-STAT signaling in the pathogenesis of IBD and the therapeutic landscape of JAK inhibitors for the treatment of IBD. Full article
(This article belongs to the Special Issue Kinases Signaling in Cancers)
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20 pages, 1745 KiB  
Review
Copper-Dependent Kinases and Their Role in Cancer Inception, Progression and Metastasis
by Alessandra Vitaliti, Anastasia De Luca and Luisa Rossi
Biomolecules 2022, 12(10), 1520; https://0-doi-org.brum.beds.ac.uk/10.3390/biom12101520 - 20 Oct 2022
Cited by 8 | Viewed by 2661
Abstract
In recent years, copper function has been expanded beyond its consolidated role as a cofactor of enzyme catalysis. Recent papers have demonstrated a new dynamic role for copper in the regulation of cell signaling pathways through direct interaction with protein kinases, modulating their [...] Read more.
In recent years, copper function has been expanded beyond its consolidated role as a cofactor of enzyme catalysis. Recent papers have demonstrated a new dynamic role for copper in the regulation of cell signaling pathways through direct interaction with protein kinases, modulating their activity. The activation of these pathways is exacerbated in cancer cells to sustain the different steps of tumor growth and dissemination. This review will focus on a novel proposed role for the transition metal copper as a regulator of cell signaling pathways through direct interaction with known protein kinases, which exhibit binding domains for this metal. Activation of these pathways in cancer cells supports both tumor growth and dissemination. In addition to the description of the results recently reported in the literature on the subject, relevance will be given to the possibility of controlling the cellular levels of copper and its homeostatic regulators. Overall, these findings may be of central relevance in order to propose copper and its homeostatic regulators as possible targets for novel therapies, which may act synergistically to those already existing to control cancer growth and dissemination. Full article
(This article belongs to the Special Issue Kinases Signaling in Cancers)
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13 pages, 1088 KiB  
Review
The Translational Regulation in mTOR Pathway
by Miaomiao Yang, Yanming Lu, Weilan Piao and Hua Jin
Biomolecules 2022, 12(6), 802; https://0-doi-org.brum.beds.ac.uk/10.3390/biom12060802 - 8 Jun 2022
Cited by 30 | Viewed by 7559
Abstract
The mechanistic/mammalian target of rapamycin (mTOR) plays a master role in cell proliferation and growth in response to insulin, amino acids, energy levels, and oxygen. mTOR can coordinate upstream signals with downstream effectors, including transcriptional and translational apparatuses to regulate fundamental cellular processes [...] Read more.
The mechanistic/mammalian target of rapamycin (mTOR) plays a master role in cell proliferation and growth in response to insulin, amino acids, energy levels, and oxygen. mTOR can coordinate upstream signals with downstream effectors, including transcriptional and translational apparatuses to regulate fundamental cellular processes such as energy utilization, protein synthesis, autophagy, cell growth, and proliferation. Of the above, protein synthesis is highly energy-consuming; thus, mRNA translation is under the tight and immediate control of mTOR signaling. The translational regulation driven by mTOR signaling mainly relies on eukaryotic translation initiation factor 4E (eIF4E)-binding protein (4E-BP), ribosomal protein S6 kinase (S6K), and its downstream players, which are significant in rapid cellular response to environmental change. mTOR signaling not only controls the general mRNA translation, but preferential mRNA translation as well. This means that mTOR signaling shows the stronger selectivity to particular target mRNAs. Some evidence has supported the contribution of 4E-BP and La-related proteins 1 (LARP1) to such translational regulation. In this review, we summarize the mTOR pathway and mainly focus on mTOR-mediated mRNA translational regulation. We introduce the major components of mTOR signaling and their functions in translational control in a general or particular manner, and describe how the specificity of regulation is coordinated. Furthermore, we summarize recent research progress and propose additional ideas for reference. Because the mTOR pathway is on the center of cell growth and metabolism, comprehensively understanding this pathway will contribute to the therapy of related diseases, including cancers, type 2 diabetes, obesity, and neurodegeneration. Full article
(This article belongs to the Special Issue Kinases Signaling in Cancers)
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