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Calcium Signalling in Cancer
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Calcium Signalling in Cancer

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (20 December 2020) | Viewed by 10336

Special Issue Editor

Dr. Iman Azimi

E-Mail Website
Guest Editor
School of Pharmacy and Pharmacology, University of Tasmania, Hobart, TAS, Australia
Interests: calcium signaling; cancer, store-operated calcium entry; breast cancer; brain cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The calcium ion (Ca2+) is an intracellular second messenger involved in diverse cellular processes, including gene transcription, cell growth and death, differentiation, metabolism, muscle contraction, and neuronal plasticity. Intracellular Ca2+ signals are specific in magnitude, time course and location, and are controlled by various components of the calcium signaling toolkit including Ca2+ channels, pumps, exchangers, and regulators. In addition to its various physiological roles, Ca2+ signaling is also involved in pathological conditions including cancer. Indeed, Ca2+ is implicated in a variety of cancer-related processes including proliferation, angiogenesis, invasion, and metastasis. While the Ca2+ signal is ubiquitous, the proteins that control Ca2+ transport are highly specialized. The expression and/or activity of these proteins is frequently dysregulated in different types of cancers where they promote specific oncogenic processes. Understanding the role of these proteins in cancer provides critical information about cancer biology and may pave the way for the development of novel therapeutic approaches.

This Special Issue of Genes aims to present novel insights into the diverse roles of Ca2+ signaling and Ca2+ signal regulators in various types of cancer, as well as potential therapeutic and diagnostic opportunities this may provide. Contributions by experts in the field in the form of research papers and critical reviews are invited.

Dr. Iman Azimi
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. Genes 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 2600 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

  • Calcium signaling
  • Cancer
  • Calcium channels and pumps
  • Targeted therapy
  • Biomarkers

Published Papers (4 papers)

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Research

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18 pages, 3683 KiB  
Article
Calcium Signalling in Medulloblastoma: An In Silico Analysis of the Expression of Calcium Regulating Genes in Patient Samples
by Ahmed Maklad, Mohammed Sedeeq, Michael J. G. Milevskiy and Iman Azimi
Genes 2021, 12(9), 1329; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12091329 - 27 Aug 2021
Cited by 3 | Viewed by 2324
Abstract
Dysregulation in calcium signalling is implicated in several cancer-associated processes, including cell proliferation, migration, invasion and therapy resistance. Modulators of specific calcium-regulating proteins have been proposed as promising future therapeutic agents for some cancers. Alterations in calcium signalling have been extensively studied in [...] Read more.
Dysregulation in calcium signalling is implicated in several cancer-associated processes, including cell proliferation, migration, invasion and therapy resistance. Modulators of specific calcium-regulating proteins have been proposed as promising future therapeutic agents for some cancers. Alterations in calcium signalling have been extensively studied in some cancers; however, this area of research is highly underexplored in medulloblastoma (MB), the most common paediatric malignant brain tumour. Current MB treatment modalities are not completely effective and can result in several long-lasting mental complications. Hence, new treatment strategies are needed. In this study, we sought to probe the landscape of calcium signalling regulators to uncover those most likely to be involved in MB tumours. We investigated the expression of calcium signalling regulator genes in MB patients using publicly available datasets. We stratified the expression level of these genes with MB molecular subgroups, tumour metastasis and patient survival to uncover correlations with clinical features. Of particular interest was CACNA1 genes, in which we were able to show a developmentally-driven change in expression within the cerebellum, MB’s tissue of origin, highlighting a potential influence on tumour incidence. This study lays a platform for future investigations into molecular regulators of calcium signalling in MB formation and progression. Full article
(This article belongs to the Special Issue Calcium Signalling in Cancer)
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21 pages, 4759 KiB  
Article
Biological Regulatory Network (BRN) Analysis and Molecular Docking Simulations to Probe the Modulation of IP3R Mediated Ca2+ Signaling in Cancer
by Humaira Ismatullah, Ishrat Jabeen and Muhammad Tariq Saeed
Genes 2021, 12(1), 34; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12010034 - 29 Dec 2020
Cited by 4 | Viewed by 2975
Abstract
Inositol trisphosphate receptor (IP3R) mediated Ca+2 signaling is essential in determining the cell fate by regulating numerous cellular processes, including cell division and cell death. Despite extensive studies about the characterization of IP3R in cancer, the underlying molecular [...] Read more.
Inositol trisphosphate receptor (IP3R) mediated Ca+2 signaling is essential in determining the cell fate by regulating numerous cellular processes, including cell division and cell death. Despite extensive studies about the characterization of IP3R in cancer, the underlying molecular mechanism initiating the cell proliferation and apoptosis remained enigmatic. Moreover, in cancer, the modulation of IP3R in downstream signaling pathways, which control oncogenesis and cancer progression, is not well characterized. Here, we constructed a biological regulatory network (BRN), and describe the remodeling of IP3R mediated Ca2+ signaling as a central key that controls the cellular processes in cancer. Moreover, we summarize how the inhibition of IP3R affects the deregulated cell proliferation and cell death in cancer cells and results in the initiation of pro-survival responses in resistance of cell death in normal cells. Further, we also investigated the role of stereo-specificity of IP3 molecule and its analogs in binding with the IP3 receptor. Molecular docking simulations showed that the hydroxyl group at R6 position along with the phosphate group at R5 position in ‘R’ conformation is more favorable for IP3 interactions. Additionally, Arg-266 and Arg-510 showed π–π and hydrogen bond interactions and Ser-278 forms hydrogen bond interactions with the IP3 binding site. Thus, they are identified as crucial for the binding of antagonists. Full article
(This article belongs to the Special Issue Calcium Signalling in Cancer)
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Review

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9 pages, 516 KiB  
Review
Store-Independent Calcium Entry and Related Signaling Pathways in Breast Cancer
by Mohamed Chamlali, Lise Rodat-Despoix and Halima Ouadid-Ahidouch
Genes 2021, 12(7), 994; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12070994 - 29 Jun 2021
Cited by 10 | Viewed by 2040
Abstract
Known as a key effector in breast cancer (BC) progression, calcium (Ca2+) is tightly regulated to maintain the desired concentration to fine-tune cell functions. Ca2+ channels are the main actors among Ca2+ transporters that control the intracellular Ca2+ [...] Read more.
Known as a key effector in breast cancer (BC) progression, calcium (Ca2+) is tightly regulated to maintain the desired concentration to fine-tune cell functions. Ca2+ channels are the main actors among Ca2+ transporters that control the intracellular Ca2+ concentration in cells. It is well known that the basal Ca2+ concentration is regulated by both store-dependent and independent Ca2+ channels in BC development and progression. However, most of the literature has reported the role of store-dependent Ca2+ entry, and only a few studies are focusing on store-independent Ca2+ entry (SICE). In this review, we aim to summarize all findings on SICE in the BC progression field. Full article
(This article belongs to the Special Issue Calcium Signalling in Cancer)
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12 pages, 533 KiB  
Review
Role of Sigma-1 Receptor in Calcium Modulation: Possible Involvement in Cancer
by Ilaria Pontisso and Laurent Combettes
Genes 2021, 12(2), 139; https://0-doi-org.brum.beds.ac.uk/10.3390/genes12020139 - 22 Jan 2021
Cited by 13 | Viewed by 2461
Abstract
Ca2+ signaling plays a pivotal role in the control of cellular homeostasis and aberrant regulation of Ca2+ fluxes have a strong impact on cellular functioning. As a consequence of this ubiquitous role, Ca2+ signaling dysregulation is involved in the pathophysiology [...] Read more.
Ca2+ signaling plays a pivotal role in the control of cellular homeostasis and aberrant regulation of Ca2+ fluxes have a strong impact on cellular functioning. As a consequence of this ubiquitous role, Ca2+ signaling dysregulation is involved in the pathophysiology of multiple diseases including cancer. Indeed, multiple studies have highlighted the role of Ca2+ fluxes in all the steps of cancer progression. In particular, the transfer of Ca2+ at the ER-mitochondrial contact sites, also known as mitochondrial associated membranes (MAMs), has been shown to be crucial for cancer cell survival. One of the proteins enriched at this site is the sigma-1 receptor (S1R), a protein that has been described as a Ca2+-sensitive chaperone that exerts a protective function in cells in various ways, including the modulation of Ca2+ signaling. Interestingly, S1R is overexpressed in many types of cancer even though the exact mechanisms by which it promotes cell survival are not fully elucidated. This review summarizes the findings describing the roles of S1R in the control of Ca2+ signaling and its involvement in cancer progression. Full article
(This article belongs to the Special Issue Calcium Signalling in Cancer)
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