Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
7.8
5.6
Journals
IJMS
Special Issues
Calcium Signaling and Calcium Transport in Tumors
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Calcium Signaling and Calcium Transport in Tumors

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 (31 January 2023) | Viewed by 7117

Special Issue Editor

Prof. Dr. Olga Krizanova

E-Mail Website
Guest Editor
Institute of Clinical and Translational Research, Biomedical Research Center, Slovak Academy of Sciences, Dubravska cesta 9, 845 45 Bratislava, Slovakia
Interests: calcium signaling; sodium/calcium exchanger; inositol 1,4,5-trisphosphate receptors; solid tumors; sulfide signaling; H2S

Special Issue Information

Dear Colleagues,

Cancer is a diverse group of diseases, where the common denominator is deregulation of diverse signaling pathways in the cell. Individual types of tumors respond differently to various chemotherapeutics, which might be due to upregulation or downregulation of different signaling pathways. Calcium, as an important signaling molecule and second messenger, regulates a wide variety of processes in the cells. For signaling, a local increase in the calcium level at a certain time and place is extremely important. This increase is realized predominantly by the selected calcium transporters localized on the plasma membrane or intracellular organelles. Thus, modulation of calcium transport systems might form another important tool for inducing apoptosis in cancer cells.

This Special Issue is focused on all aspects of calcium flux through calcium transport systems in cancer cells. We would like to focus predominantly on different types of solid tumors. We aim to provide a complex view on calcium transport not only in respect to tumor growth and invasiveness, but also in respect to tumor treatment.

Prof. Dr. Olga Krizanova
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

  • Calcium signaling
  • Calcium transport
  • Ion channels
  • Membrane receptors
  • Cancer
  • Stable cell lines
  • Proliferation
  • Migration
  • Apoptosis

Published Papers (3 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

16 pages, 2790 KiB  
Article
The p53 and Calcium Regulated Actin Rearrangement in Model Cells
by Alexandra Hencz, Edina Szabó-Meleg, Muhammad Yaqoob Dayo, Ardora Bilibani, Szilvia Barkó, Miklós Nyitrai and Dávid Szatmári
Int. J. Mol. Sci. 2022, 23(16), 9078; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23169078 - 13 Aug 2022
Cited by 1 | Viewed by 1717
Abstract
Long-term cellular stress maintains high intracellular Ca2+ concentrations which ultimately initiates apoptosis. Our interest is focused on how the gelsolin (GSN) and junctional mediating and regulating Y protein (JMY) play important roles in stress response. Both of these proteins can bind p53 [...] Read more.
Long-term cellular stress maintains high intracellular Ca2+ concentrations which ultimately initiates apoptosis. Our interest is focused on how the gelsolin (GSN) and junctional mediating and regulating Y protein (JMY) play important roles in stress response. Both of these proteins can bind p53 and actin. We investigated using in vitro fluorescence spectroscopy and found that the p53 competes with actin in GSN to inhibit p53–JMY complex formation. A high Ca2+ level initializes p53 dimerization; the dimer competes with actin on JMY, which can lead to p53–JMY cotransport into the nucleus. Here we investigated how the motility and division rate of HeLa cells changes due to low-voltage electroporation of GSN or JMY in scratching assays. We revealed that JMY inhibits their motion, but that it can accelerate the cell division. GSN treatment slows down cell division but does not affect cell motility. HeLa cells fully recovered the gap 20 h after the electroporation with JMY and then started to release from the glass slides. Taken together, our in vitro results indicate that GSN and JMY may play an important role in the cellular stress response. Full article
(This article belongs to the Special Issue Calcium Signaling and Calcium Transport in Tumors)
►▼ Show Figures

Figure 1

14 pages, 2006 KiB  
Article
ORAI1-Regulated Gene Expression in Breast Cancer Cells: Roles for STIM1 Binding, Calcium Influx and Transcription Factor Translocation
by Mélanie Robitaille, Shao Ming Chan, Amelia A. Peters, Limin Dai, Choon Leng So, Alice H. L. Bong, Francisco Sadras, Sarah J. Roberts-Thomson and Gregory R. Monteith
Int. J. Mol. Sci. 2022, 23(11), 5867; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23115867 - 24 May 2022
Cited by 3 | Viewed by 2070
Abstract
A remodeling of calcium homeostasis, including calcium influx via store-operated calcium entry (SOCE), is a feature of breast cancers. SOCE is critical to maintain calcium balance in the endoplasmic reticulum calcium store and is an important mechanism for calcium signaling in a variety [...] Read more.
A remodeling of calcium homeostasis, including calcium influx via store-operated calcium entry (SOCE), is a feature of breast cancers. SOCE is critical to maintain calcium balance in the endoplasmic reticulum calcium store and is an important mechanism for calcium signaling in a variety of cell types, including breast cancer cells. The canonical mechanism of SOCE is stromal interacting molecule 1 (STIM1)-mediated activation of ORAI. Elevated ORAI1 expression is a feature of basal breast cancer cells. However, the role of ORAI1 in the regulation of transcription in breast cancer cells of the basal molecular subtype is still unclear. Using CRISPR-Cas9 gene editing, ORAI1 protein expression was disrupted in MDA-MB-231 and MDA-MB-468 basal breast cancer cells. The ORAI1 wild-type and mutants were reintroduced into ORAI1 knockout cells to study the role of ORAI1 in gene transcriptional regulation. In the absence of calcium store depletion, ORAI1 regulated PTGS2 in MDA-MB-231 cells, and this was dependent on ORAI1 pore function and STIM1 binding. The activation of SOCE by thapsigargin resulted in ORAI1-dependent increases in IL6 transcription in MDA-MB-468 cells; this was also dependent on ORAI1 pore function and STIM1 binding and was associated with the translocation of NFAT1. Given the upregulation of ORAI1 in basal breast cancer cells, our results provide further evidence that ORAI1 may contribute to cancer progression through regulation of gene expression. Full article
(This article belongs to the Special Issue Calcium Signaling and Calcium Transport in Tumors)
►▼ Show Figures

Figure 1

14 pages, 3962 KiB  
Article
Activation of the Ion Channel TRPV4 Induces Epithelial to Mesenchymal Transition in Breast Cancer Cells
by Iman Azimi, Mélanie Robitaille, Kaela Armitage, Choon Leng So, Michael J. G. Milevskiy, Korinne Northwood, Huai Fang Lim, Erik W. Thompson, Sarah J. Roberts-Thomson and Gregory R. Monteith
Int. J. Mol. Sci. 2020, 21(24), 9417; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21249417 - 10 Dec 2020
Cited by 19 | Viewed by 2691
Abstract
Epithelial to mesenchymal transition (EMT) in cancer is important in therapeutic resistance and invasiveness. Calcium signaling is key to the induction of EMT in breast cancer cells. Although inhibition of specific calcium-permeable ion channels regulates the induction of a sub-set of EMT markers [...] Read more.
Epithelial to mesenchymal transition (EMT) in cancer is important in therapeutic resistance and invasiveness. Calcium signaling is key to the induction of EMT in breast cancer cells. Although inhibition of specific calcium-permeable ion channels regulates the induction of a sub-set of EMT markers in breast cancer cells, it is still unclear if activation of a specific calcium channel can be a driver for the induction of EMT events. In this study, we exploited the availability of a selective pharmacological activator of the calcium-permeable ion channel TRPV4 to assess the direct role of calcium influx in EMT marker induction. Gene association studies revealed a link between TRPV4 and gene-ontologies associated with EMT and poorer relapse-free survival in lymph node-positive basal breast cancers. TRPV4 was an important component of the calcium influx phase induced in MDA-MB-468 breast cancer cells by the EMT inducer epidermal growth factor (EGF). Pharmacological activation of TRPV4 then drove the induction of a variety of EMT markers in breast cancer cells. These studies demonstrate that calcium influx through specific pathways appears to be sufficient to trigger EMT events. Full article
(This article belongs to the Special Issue Calcium Signaling and Calcium Transport in Tumors)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop