Targeting Channel Proteins in Cancer

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

Deadline for manuscript submissions: closed (15 January 2024) | Viewed by 4616

Special Issue Editor


E-Mail Website
Guest Editor
Laboratory of Cell and Molecular Physiology (LPCM), UR UPJV4667, Université de Picardie Jules Verne, Amiens, France
Interests: potassium channels; calcium channels; cancer cells; breast cancer; hypoxia; cell migration; metastasis; cell models

Special Issue Information

Dear Colleagues, 

Ion channels are crucial proteins regulating all cell functions in physiology or pathological conditions. Their involvement in cancer promotion is progressively elucidated but it is necessary to deeply understand underlying mechanisms to use them as targets. Function or expression modification, localization or addressing, complex formation, microenvironment interaction, genetic regulation, or downstream signaling pathways are different processes related to ion channels altered in cancer cells and promote tumor development. In addition, other cells surrounding the tumor could show ion channel alteration promoting cancer evolution.

Despite all the information already available, ion channels have not yet reached their full clinical value in the cancer field. This Special Issue will highlight all the new elements allowing the use of ion channels as therapeutic targets to fight against cancer development, covering both basic and more preclinical aspects.

Dr. Alban Girault
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. 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

  • ion channels
  • cancer cells
  • therapeutic target
  • Ca2+ signaling
  • cancer therapy

Published Papers (2 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Review

21 pages, 982 KiB  
Review
The Phosphorylation of Kv1.3: A Modulatory Mechanism for a Multifunctional Ion Channel
by María Navarro-Pérez, Irene Estadella, Anna Benavente-Garcia, Ruth Orellana-Fernández, Anna Petit, Joan Carles Ferreres and Antonio Felipe
Cancers 2023, 15(10), 2716; https://doi.org/10.3390/cancers15102716 - 11 May 2023
Cited by 1 | Viewed by 2109
Abstract
The voltage-gated potassium channel Kv1.3 plays a pivotal role in a myriad of biological processes, including cell proliferation, differentiation, and apoptosis. Kv1.3 undergoes fine-tuned regulation, and its altered expression or function correlates with tumorigenesis and cancer progression. Moreover, posttranslational modifications (PTMs), such as [...] Read more.
The voltage-gated potassium channel Kv1.3 plays a pivotal role in a myriad of biological processes, including cell proliferation, differentiation, and apoptosis. Kv1.3 undergoes fine-tuned regulation, and its altered expression or function correlates with tumorigenesis and cancer progression. Moreover, posttranslational modifications (PTMs), such as phosphorylation, have evolved as rapid switch-like moieties that tightly modulate channel activity. In addition, kinases are promising targets in anticancer therapies. The diverse serine/threonine and tyrosine kinases function on Kv1.3 and the effects of its phosphorylation vary depending on multiple factors. For instance, Kv1.3 regulatory subunits (KCNE4 and Kvβ) can be phosphorylated, increasing the complexity of channel modulation. Scaffold proteins allow the Kv1.3 channelosome and kinase to form protein complexes, thereby favoring the attachment of phosphate groups. This review compiles the network triggers and signaling pathways that culminate in Kv1.3 phosphorylation. Alterations to Kv1.3 expression and its phosphorylation are detailed, emphasizing the importance of this channel as an anticancer target. Overall, further research on Kv1.3 kinase-dependent effects should be addressed to develop effective antineoplastic drugs while minimizing side effects. This promising field encourages basic cancer research while inspiring new therapy development. Full article
(This article belongs to the Special Issue Targeting Channel Proteins in Cancer)
Show Figures

Figure 1

49 pages, 6528 KiB  
Review
CRAC and SK Channels: Their Molecular Mechanisms Associated with Cancer Cell Development
by Adéla Tiffner, Valentina Hopl and Isabella Derler
Cancers 2023, 15(1), 101; https://doi.org/10.3390/cancers15010101 - 23 Dec 2022
Cited by 6 | Viewed by 2037
Abstract
Cancer represents a major health burden worldwide. Several molecular targets have been discovered alongside treatments with positive clinical outcomes. However, the reoccurrence of cancer due to therapy resistance remains the primary cause of mortality. Endeavors in pinpointing new markers as molecular targets in [...] Read more.
Cancer represents a major health burden worldwide. Several molecular targets have been discovered alongside treatments with positive clinical outcomes. However, the reoccurrence of cancer due to therapy resistance remains the primary cause of mortality. Endeavors in pinpointing new markers as molecular targets in cancer therapy are highly desired. The significance of the co-regulation of Ca2+-permeating and Ca2+-regulated ion channels in cancer cell development, proliferation, and migration make them promising molecular targets in cancer therapy. In particular, the co-regulation of the Orai1 and SK3 channels has been well-studied in breast and colon cancer cells, where it finally leads to an invasion-metastasis cascade. Nevertheless, many questions remain unanswered, such as which key molecular components determine and regulate their interplay. To provide a solid foundation for a better understanding of this ion channel co-regulation in cancer, we first shed light on the physiological role of Ca2+ and how this ion is linked to carcinogenesis. Then, we highlight the structure/function relationship of Orai1 and SK3, both individually and in concert, their role in the development of different types of cancer, and aspects that are not yet known in this context. Full article
(This article belongs to the Special Issue Targeting Channel Proteins in Cancer)
Show Figures

Figure 1

Back to TopTop