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Ion Channels as Therapeutic Target in Cancer
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Ion Channels as Therapeutic Target in Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (30 September 2022) | Viewed by 5845

Special Issue Editor

Prof. Dr. Jean-François Desaphy

E-Mail Website
Guest Editor
Department of Biomedical Sciences and Human oncology, School of Medicine, University of Bari Aldo Moror, Bari, Italy
Interests: ion channels; ion channelopathies; rare diseases; cancer; pharmacogenetics; precision medicine; drug discovery; drug repositioning
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer is the second leading cause of death worldwide. Despite the constant progress in cancer treatment, there is still a need to find new druggable targets. Ion channels constitute an important family of membrane carriers involved in most, if not all, cellular functions, while ion channel dysfunction is a major event in many diseases. The human genome contains more than 400 genes encoding ion channel subunits; alternative splicing and heteromeric subunit assembly both tremendously increase the variety of ion channels. Approximately 5% of marketed drugs are targeting ion channels, addressing mostly diseases characterized by altered cell membrane excitability. More recently, more attention has been paid to the “non-canonical” roles of ion channels in cell cycle progression, differentiation, survival, and death, especially in cancer cells. They may be involved in the control or sensing of the tumor microenvironment, and they may also modulate intracellular signaling. This makes ion channels promising targets to fight cancer through drug repositioning, the discovery of new pharmacological agents, and possibly the use of target therapies including monoclonal antibodies.

The aim of this Special Issue is to publish original papers and reviews dealing with the role of ion channels in cancer progression and therapy.

Prof. Dr. Jean-François Desaphy
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • cancer
  • ion channels
  • cell membrane
  • intracellular ion channels
  • drug targets
  • target therapy
  • tumor microenvironment
  • intracellular signaling
  • tumor aggressiveness
  • tumor progression
  • apoptosis
  • metastasis
  • drug resistance

Published Papers (3 papers)

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Research

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15 pages, 1634 KiB  
Article
ECM Composition Differentially Regulates Intracellular and Extracellular pH in Normal and Cancer Pancreatic Duct Epithelial Cells
by Daria Di Molfetta, Stefania Cannone, Maria Raffaella Greco, Rosa Caroppo, Francesca Piccapane, Tiago Miguel Amaral Carvalho, Concetta Altamura, Ilaria Saltarella, Diana Tavares Valente, Jean Francois Desaphy, Stephan J. Reshkin and Rosa Angela Cardone
Int. J. Mol. Sci. 2023, 24(13), 10632; https://doi.org/10.3390/ijms241310632 - 25 Jun 2023
Viewed by 1417
Abstract
Intracellular pH (pHi) regulation is a challenge for the exocrine pancreas, where the luminal secretion of bicarbonate-rich fluid is accompanied by interstitial flows of acid. This acid–base transport requires a plethora of ion transporters, including bicarbonate transporters and the Na+/H+ [...] Read more.
Intracellular pH (pHi) regulation is a challenge for the exocrine pancreas, where the luminal secretion of bicarbonate-rich fluid is accompanied by interstitial flows of acid. This acid–base transport requires a plethora of ion transporters, including bicarbonate transporters and the Na+/H+ exchanger isoform 1 (NHE1), which are dysregulated in Pancreatic Ductal Adenocarcinoma (PDAC). PDAC progression is favored by a Collagen-I rich extracellular matrix (ECM) which exacerbates the physiological interstitial acidosis. In organotypic cultures of normal human pancreatic cells (HPDE), parenchymal cancer cells (CPCs) and cancer stem cells (CSCs) growing on matrices reproducing ECM changes during progression, we studied resting pHi, the pHi response to fluxes of NaHCO3 and acidosis and the role of NHE1 in pHi regulation. Our findings show that: (i) on the physiological ECM, HPDE cells have the most alkaline pHi, followed by CSCs and CPCs, while a Collagen I-rich ECM reverses the acid–base balance in cancer cells compared to normal cells; (ii) both resting pHi and pHi recovery from an acid load are reduced by extracellular NaHCO3, especially in HPDE cells on a normal ECM; (iii) cancer cell NHE1 activity is less affected by NaHCO3. We conclude that ECM composition and the fluctuations of pHe cooperate to predispose pHi homeostasis towards the presence of NaHCO3 gradients similar to that expected in the tumor. Full article
(This article belongs to the Special Issue Ion Channels as Therapeutic Target in Cancer)
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17 pages, 12686 KiB  
Article
Inositol (1,4,5)-Trisphosphate Receptors in Invasive Breast Cancer: A New Prognostic Tool?
by Arthur Foulon, Pierre Rybarczyk, Nicolas Jonckheere, Eva Brabencova, Henri Sevestre, Halima Ouadid-Ahidouch and Lise Rodat-Despoix
Int. J. Mol. Sci. 2022, 23(6), 2962; https://doi.org/10.3390/ijms23062962 - 9 Mar 2022
Cited by 5 | Viewed by 2100
Abstract
Breast cancer is the leading cause of cancer death among women in worldwide and France. The disease prognosis and treatment differ from one breast cancer subtype to another, and the disease outcome depends on many prognostic factors. Deregulation of ion flux (especially Ca [...] Read more.
Breast cancer is the leading cause of cancer death among women in worldwide and France. The disease prognosis and treatment differ from one breast cancer subtype to another, and the disease outcome depends on many prognostic factors. Deregulation of ion flux (especially Ca2+ flux) is involved in many pathophysiology processes, including carcinogenesis. Inside the cell, the inositol-trisphosphate receptor (IP3R) is a major player in the regulation of the Ca2+ flux from the endoplasmic reticulum to the cytoplasm. The IP3Rs (and particularly the IP3R3 subtype) are known to be involved in proliferation, migration, and invasion processes in breast cancer cell lines. The objective of the present study was to evaluate the potential value of IP3Rs as prognostic biomarkers in breast cancer. We found that expression levels of IP3R3 and IP3R1 (but not IP3R2) were significantly higher in invasive breast cancer of no special type than in non-tumor tissue from the same patient. However, the IP3R3 subtype was expressed more strongly than the IP3R1 and IP3R2 subtypes. Furthermore, the expression of IP3R3 (but not of IP3R1 or IP3R2) was positively correlated with prognostic factors such as tumor size, regional node invasion, histologic grade, proliferation index, and hormone receptor status. In an analysis of public databases, we found that all IP3Rs types are significantly associated with overall survival and progression-free survival in patients with breast cancer. We conclude that relative to the other two IP3R subtypes, IP3R3 expression is upregulated in breast cancer and is correlated with prognostic factors. Full article
(This article belongs to the Special Issue Ion Channels as Therapeutic Target in Cancer)
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Review

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14 pages, 770 KiB  
Review
Ion Channels in Multiple Myeloma: Pathogenic Role and Therapeutic Perspectives
by Ilaria Saltarella, Concetta Altamura, Aurelia Lamanuzzi, Benedetta Apollonio, Angelo Vacca, Maria Antonia Frassanito and Jean-François Desaphy
Int. J. Mol. Sci. 2022, 23(13), 7302; https://doi.org/10.3390/ijms23137302 - 30 Jun 2022
Viewed by 1731
Abstract
Ion channels are pore-forming proteins that allow ions to flow across plasma membranes and intracellular organelles in both excitable and non-excitable cells. They are involved in the regulation of several biological processes (i.e., proliferation, cell volume and shape, differentiation, migration, and apoptosis). Recently, [...] Read more.
Ion channels are pore-forming proteins that allow ions to flow across plasma membranes and intracellular organelles in both excitable and non-excitable cells. They are involved in the regulation of several biological processes (i.e., proliferation, cell volume and shape, differentiation, migration, and apoptosis). Recently, the aberrant expression of ion channels has emerged as an important step of malignant transformation, tumor progression, and drug resistance, leading to the idea of “onco-channelopathy”. Here, we review the contribution of ion channels and transporters in multiple myeloma (MM), a hematological neoplasia characterized by the expansion of tumor plasma cells (MM cells) in the bone marrow (BM). Deregulation of ion channels sustains MM progression by modulating intracellular pathways that promote MM cells’ survival, proliferation, and drug resistance. Finally, we focus on the promising role of ion channels as therapeutic targets for the treatment of MM patients in a combination strategy with currently used anti-MM drugs to improve their cytotoxic activity and reduce adverse effects. Full article
(This article belongs to the Special Issue Ion Channels as Therapeutic Target in Cancer)
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