Kinases in Cancer and Other Diseases, 2nd Edition

Topic Information

Dear Colleagues,

Protein kinases comprise a large family of enzymes that catalyze protein phosphorylation. The human genome contains 518 protein kinase genes. Phosphorylation is one of the major mechanisms for regulating various cellular processes, such as proliferation, the apoptosis cell cycle, growth, apoptosis, differentiation, etc. The deregulation of kinase activity can result in significant changes in these processes. Furthermore, deregulated kinases are often oncogenic and essential for the survival and spreading of cancer cells. There are different ways in which kinases are involved in cancers, including misregulated expression and/or amplification, mutation, chromosomal translocation, abnormal phosphorylation, and epigenetic regulation. In order to further investigage these functions, there are various scientific projects assessing the importance of kinases in cancers as well as several other diseases, such as polycystic kidney disease, glomerulonephritis, neurodegeneration, retinal degeneration, lung inflammation, etc. In clinical science the major two kinase investigation routes are (1) using kinases as biomarkers in cancer prognostics and diagnostics and (2) treating cancers with kinase inhibitors and/or monoclonal antibodies. This Topic will highlight current and innovative research achievements in these areas.

Dr. Jonas Cicenas
Dr. Anna M. Czarnecka
Topic Editors

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Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Biology biology	4.2	4.0	2012	18.7 Days	CHF 2700	Submit
Biomolecules biomolecules	5.5	8.3	2011	16.9 Days	CHF 2700	Submit
Cancers cancers	5.2	7.4	2009	17.9 Days	CHF 2900	Submit
Cells cells	6.0	9.0	2012	16.6 Days	CHF 2700	Submit
International Journal of Molecular Sciences ijms	5.6	7.8	2000	16.3 Days	CHF 2900	Submit
Pharmaceuticals pharmaceuticals	4.6	4.7	2004	14.6 Days	CHF 2900	Submit

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Published Papers (3 papers)

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All Biology Biomolecules Cancers Cells IJMS Pharmaceuticals

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6 pages, 1193 KiB  

Open AccessEditorial

CDK Inhibitors and FDA: Approved and Orphan

by Jonas Cicenas and Jokubas Simkus

Cancers 2024, 16(8), 1555; https://doi.org/10.3390/cancers16081555 - 19 Apr 2024

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Abstract

The protein kinases are a large family of enzymes which catalyze protein phosphorylation at certain amino acids [...] Full article

(This article belongs to the Topic Kinases in Cancer and Other Diseases, 2nd Edition)

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36 pages, 4065 KiB  

Open AccessReview

The Mitochondrial Connection: The Nek Kinases’ New Functional Axis in Mitochondrial Homeostasis

by Fernanda L. Basei, Ivan Rosa e Silva, Pedro R. Firmino Dias, Camila C. Ferezin, Andressa Peres de Oliveira, Luidy K. Issayama, Livia A. R. Moura, Fernando Riback da Silva and Jörg Kobarg

Cells 2024, 13(6), 473; https://doi.org/10.3390/cells13060473 - 07 Mar 2024

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Abstract

Mitochondria provide energy for all cellular processes, including reactions associated with cell cycle progression, DNA damage repair, and cilia formation. Moreover, mitochondria participate in cell fate decisions between death and survival. Nek family members have already been implicated in DNA damage response, cilia [...] Read more.

Mitochondria provide energy for all cellular processes, including reactions associated with cell cycle progression, DNA damage repair, and cilia formation. Moreover, mitochondria participate in cell fate decisions between death and survival. Nek family members have already been implicated in DNA damage response, cilia formation, cell death, and cell cycle control. Here, we discuss the role of several Nek family members, namely Nek1, Nek4, Nek5, Nek6, and Nek10, which are not exclusively dedicated to cell cycle-related functions, in controlling mitochondrial functions. Specifically, we review the function of these Neks in mitochondrial respiration and dynamics, mtDNA maintenance, stress response, and cell death. Finally, we discuss the interplay of other cell cycle kinases in mitochondrial function and vice versa. Nek1, Nek5, and Nek6 are connected to the stress response, including ROS control, mtDNA repair, autophagy, and apoptosis. Nek4, in turn, seems to be related to mitochondrial dynamics, while Nek10 is involved with mitochondrial metabolism. Here, we propose that the participation of Neks in mitochondrial roles is a new functional axis for the Nek family. Full article

(This article belongs to the Topic Kinases in Cancer and Other Diseases, 2nd Edition)

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Open AccessArticle

The CDK Inhibitor Dinaciclib Improves Cisplatin Response in Nonseminomatous Testicular Cancer: A Preclinical Study

by Elisa Rossini, Mariangela Tamburello, Andrea Abate, Silvia Zini, Giovanni Ribaudo, Alessandra Gianoncelli, Stefano Calza, Francesca Valcamonico, Nazareno R. Suardi, Giuseppe Mirabella, Alfredo Berruti and Sandra Sigala

Cells 2024, 13(5), 368; https://doi.org/10.3390/cells13050368 - 20 Feb 2024

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Abstract

Background: Most patients with testicular germ cell tumors (GCTs) are treated with cisplatin (CP)-based chemotherapy. However, some of them may develop CP resistance and therefore represent a clinical challenge. Cyclin-dependent kinase 5 (CDK5) is involved in chemotherapy resistance in different types of cancer. [...] Read more.

Background: Most patients with testicular germ cell tumors (GCTs) are treated with cisplatin (CP)-based chemotherapy. However, some of them may develop CP resistance and therefore represent a clinical challenge. Cyclin-dependent kinase 5 (CDK5) is involved in chemotherapy resistance in different types of cancer. Here, we investigated the possible role of CDK5 and other CDKs targeted by dinaciclib in nonseminoma cell models (both CP-sensitive and CP-resistant), evaluating the potential of the CDK inhibitor dinaciclib as a single/combined agent for the treatment of advanced/metastatic testicular cancer (TC). Methods: The effects of dinaciclib and CP on sensitive and resistant NT2/D1 and NCCIT cell viability and proliferation were evaluated using MTT assays and direct count methods. Flow cytometry cell-cycle analysis was performed. The protein expression was assessed via Western blotting. The in vivo experiments were conducted in zebrafish embryos xenografted with TC cells. Results: Among all the CDKs analyzed, CDK5 protein expression was significantly higher in CP-resistant models. Dinaciclib reduced the cell viability and proliferation in each cell model, inducing changes in cell-cycle distribution. In drug combination experiments, dinaciclib enhances the CP effect both in vitro and in the zebrafish model. Conclusions: Dinaciclib, when combined with CP, could be useful for improving nonseminoma TC response to CP. Full article

(This article belongs to the Topic Kinases in Cancer and Other Diseases, 2nd Edition)

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