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Calcium Channel Regulation in Cancer: Unravelling the Molecular Mechanisms beneath the Membrane

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

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 11551

Special Issue Editor

Dr. Dimitra Gkika

E-Mail Website
Guest Editor
CANcer Heterogeneity, Plasticity and Resistance to THERapies Lab, Faculty of Sciences and Technologies, University of Lille, 59000 Lille, France
Interests: ion channel; TRP channel; calcium homeostasis; cancer; angiogenesis; small GTPases; androgen receptor; steroid fast non genomic actions; expression profile; cell migration; cell adhesion

Special Issue Information

Dear Colleagues,

Over the last decades, an increasing number of calcium channels located at the cell surface or inner membranes, including voltage-dependent calcium channels (VDCC), transient receptor potential (TRP), store-operated calcium (SOC) channels, the inositol 1,4,5-trisphosphate receptor (IP3R), and mitochondrial calcium uniporter (MCU), have been suggested as clinical markers and/or therapeutical targets for cancer. In this perspective, major advances have contributed to a deeper understanding of the regulatory mechanisms controlling the channel activity, as well as its consequences in tumour initiation, growth, and metastasis.

I therefore would like to invite you to participate in this Special Issue, "Calcium Channel Regulation in Cancer: Unravelling the Molecular Mechanisms beneath the Membrane", by presenting your most recent research or ideas about intracellular factors such as channel associated factors, kinases, partner proteins, small GTPases, calcium binding proteins, signalling molecules affecting channel functioning, and the consequential major aspects of carcinogenesis.

Assoc. Prof. Dimitra Gkika
Guest Editor

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Keywords

  • ion channel
  • calcium signalling
  • partner protein
  • protein–protein interaction
  • TRP channel
  • channel subunit
  • TRP
  • ORAI
  • CaV
  • IP3R
  • MCU
  • cancer
  • tumour initiation
  • tumour growth
  • metastasis

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Published Papers (3 papers)

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20 pages, 4497 KiB  
Article
Involvement of ORAI1/SOCE in Human AML Cell Lines and Primary Cells According to ABCB1 Activity, LSC Compartment and Potential Resistance to Ara-C Exposure
by Clara Lewuillon, Aurélie Guillemette, Sofia Titah, Faruk Azam Shaik, Nathalie Jouy, Ossama Labiad, Valerio Farfariello, Marie-Océane Laguillaumie, Thierry Idziorek, Adeline Barthélémy, Pauline Peyrouze, Céline Berthon, Mehmet Cagatay Tarhan, Meyling Cheok, Bruno Quesnel, Loïc Lemonnier and Yasmine Touil
Int. J. Mol. Sci. 2022, 23(10), 5555; https://doi.org/10.3390/ijms23105555 - 16 May 2022
Cited by 4 | Viewed by 3157
Abstract
Acute myeloid leukemia (AML) is a hematological malignancy with a high risk of relapse. This issue is associated with the development of mechanisms leading to drug resistance that are not yet fully understood. In this context, we previously showed the clinical significance of [...] Read more.
Acute myeloid leukemia (AML) is a hematological malignancy with a high risk of relapse. This issue is associated with the development of mechanisms leading to drug resistance that are not yet fully understood. In this context, we previously showed the clinical significance of the ATP binding cassette subfamily B-member 1 (ABCB1) in AML patients, namely its association with stemness markers and an overall worth prognosis. Calcium signaling dysregulations affect numerous cellular functions and are associated with the development of the hallmarks of cancer. However, in AML, calcium-dependent signaling pathways remain poorly investigated. With this study, we show the involvement of the ORAI1 calcium channel in store-operated calcium entry (SOCE), the main calcium entry pathway in non-excitable cells, in two representative human AML cell lines (KG1 and U937) and in primary cells isolated from patients. Moreover, our data suggest that in these models, SOCE varies according to the differentiation status, ABCB1 activity level and leukemic stem cell (LSC) proportion. Finally, we present evidence that ORAI1 expression and SOCE amplitude are modulated during the establishment of an apoptosis resistance phenotype elicited by the chemotherapeutic drug Ara-C. Our results therefore suggest ORAI1/SOCE as potential markers of AML progression and drug resistance apparition. Full article
(This article belongs to the Special Issue Calcium Channel Regulation in Cancer: Unravelling the Molecular Mechanisms beneath the Membrane)
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16 pages, 23844 KiB  
Article
Developing a Mathematical Model of Intracellular Calcium Dynamics for Evaluating Combined Anticancer Effects of Afatinib and RP4010 in Esophageal Cancer
by Yan Chang, Marah Funk, Souvik Roy, Elizabeth Stephenson, Sangyong Choi, Hristo V. Kojouharov, Benito Chen and Zui Pan
Int. J. Mol. Sci. 2022, 23(3), 1763; https://doi.org/10.3390/ijms23031763 - 3 Feb 2022
Cited by 12 | Viewed by 2995
Abstract
Targeting dysregulated Ca2+ signaling in cancer cells is an emerging chemotherapy approach. We previously reported that store-operated Ca2+ entry (SOCE) blockers, such as RP4010, are promising antitumor drugs for esophageal cancer. As a tyrosine kinase inhibitor (TKI), afatinib received FDA approval [...] Read more.
Targeting dysregulated Ca2+ signaling in cancer cells is an emerging chemotherapy approach. We previously reported that store-operated Ca2+ entry (SOCE) blockers, such as RP4010, are promising antitumor drugs for esophageal cancer. As a tyrosine kinase inhibitor (TKI), afatinib received FDA approval to be used in targeted therapy for patients with EGFR mutation-positive cancers. While preclinical studies and clinical trials have shown that afatinib has benefits for esophageal cancer patients, it is not known whether a combination of afatinib and RP4010 could achieve better anticancer effects. Since TKI can alter intracellular Ca2+ dynamics through EGFR/phospholipase C-γ pathway, in this study, we evaluated the inhibitory effect of afatinib and RP4010 on intracellular Ca2+ oscillations in KYSE-150, a human esophageal squamous cell carcinoma cell line, using both experimental and mathematical simulations. Our mathematical simulation of Ca2+ oscillations could fit well with experimental data responding to afatinib or RP4010, both separately or in combination. Guided by simulation, we were able to identify a proper ratio of afatinib and RP4010 for combined treatment, and such a combination presented synergistic anticancer-effect evidence by experimental measurement of intracellular Ca2+ and cell proliferation. This intracellular Ca2+ dynamic-based mathematical simulation approach could be useful for a rapid and cost-effective evaluation of combined targeting therapy drugs. Full article
(This article belongs to the Special Issue Calcium Channel Regulation in Cancer: Unravelling the Molecular Mechanisms beneath the Membrane)
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Review

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11 pages, 1184 KiB  
Review
Role of Orai3 in the Pathophysiology of Cancer
by Jose Sanchez-Collado, Isaac Jardin, Jose J. López, Victor Ronco, Gines M. Salido, Charlotte Dubois, Natalia Prevarskaya and Juan A. Rosado
Int. J. Mol. Sci. 2021, 22(21), 11426; https://doi.org/10.3390/ijms222111426 - 22 Oct 2021
Cited by 11 | Viewed by 4497
Abstract
The mammalian exclusive Orai3 channel participates in the generation and/or modulation of two independent Ca2+ currents, the store-operated current, Icrac, involving functional interactions between the stromal interaction molecules (STIM), STIM1/STIM2, and Orai1/Orai2/Orai3, as well as the store-independent arachidonic acid (AA) [...] Read more.
The mammalian exclusive Orai3 channel participates in the generation and/or modulation of two independent Ca2+ currents, the store-operated current, Icrac, involving functional interactions between the stromal interaction molecules (STIM), STIM1/STIM2, and Orai1/Orai2/Orai3, as well as the store-independent arachidonic acid (AA) (or leukotriene C4)-regulated current Iarc, which involves Orai1, Orai3 and STIM1. Overexpression of functional Orai3 has been described in different neoplastic cells and cancer tissue samples as compared to non-tumor cells or normal adjacent tissue. In these cells, Orai3 exhibits a cell-specific relevance in Ca2+ influx. In estrogen receptor-positive breast cancer cells and non-small cell lung cancer (NSCLC) cells store-operated Ca2+ entry (SOCE) is strongly dependent on Orai3 expression while in colorectal cancer and pancreatic adenocarcinoma cells Orai3 predominantly modulates SOCE. On the other hand, in prostate cancer cells Orai3 expression has been associated with the formation of Orai1/Orai3 heteromeric channels regulated by AA and reduction in SOCE, thus leading to enhanced proliferation. Orai3 overexpression is associated with supporting several cancer hallmarks, including cell cycle progression, proliferation, migration, and apoptosis resistance. This review summarizes the current knowledge concerning the functional role of Orai3 in the pathogenesis of cancer. Full article
(This article belongs to the Special Issue Calcium Channel Regulation in Cancer: Unravelling the Molecular Mechanisms beneath the Membrane)
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