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Cancers
Special Issues
Calcium Signaling in Cancer Cell Progression
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Calcium Signaling in Cancer Cell Progression

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

Deadline for manuscript submissions: 30 November 2025 | Viewed by 742

Special Issue Editor

Dr. Amantini Consuelo

E-Mail Website
Guest Editor
School of Biosciences and Veterinary Medicine, Biology Division, University of Camerino, Via Gentile III da Varano, 62032 Camerino, Italy
Interests: TRP; cancer biology; apoptosis; autophagy; senescence; circulating stem cell; chemoresistance
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It is well accepted that cancer cells display modified calcium signaling to facilitate many pro-tumoral processes, such as proliferation, angiogenesis, exosome release, invasion, loss of death pathways, and responses to chemotherapy. Thus, the impairment of Ca2+ homeostasis is considered a crucial driver of cancer initiation and progression. There is ample evidence demonstrating that the alteration of the intracellular Ca2+ flux is the consequence of an aberrant expression and function of cation channels, pumps, sensors, or transporters that, therefore, represent attractive targets for the development of innovative anticancer drugs.

Recently, interorganellar Ca2+ communication is attracting a lot of attention. This is because these calcium exchanges between organelles are altered in cancer and promote tumor progression by influencing cell metabolism and cell fate.

This Special Issue aims to compile the available information we have regarding cancer on the role of Ca2+ signaling in the following areas:

- Membrane contact sites between the mitochondria and endoplasmic reticula or lysosomes.

- Interorganelle platforms connecting endosomes and plasma membranes.

- Interorganelle Ca2+ flux and cancer cell metabolism and fate.

- Alterations of membrane contact sites to promote migration and invasion.

- Mitoflash and tumor progression.

- Ca2+ interplay between organelles and exosome release.

Dr. Amantini Consuelo
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 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

  • interorganellar Ca2+ communication
  • membrane contact sites
  • tumor progression
  • intracellular Ca2+ flux
  • cation channels
  • calcium dysregulation
  • cell fate
  • targeted therapy

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Published Papers (1 paper)

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17 pages, 2739 KiB  
Article
TP53 Mutation-Specific Dysregulation of Store-Operated Calcium Entry and Apoptotic Sensitivity in Triple-Negative Breast Cancer
by Kaneez E. Rabab, Paul J. Buchanan, Grace Colley, Anita White, Aisling Murphy, Chloe McCormack and Alex J. Eustace
Cancers 2025, 17(10), 1614; https://doi.org/10.3390/cancers17101614 - 10 May 2025
Viewed by 412
Abstract
Background: Triple-negative breast cancer (TNBC) is an aggressive subtype lacking estrogen, progesterone, and HER2 receptors, and is associated with poor prognosis and limited targeted therapeutic options. TP53 mutations occur in the majority of TNBC cases, disrupting p53’s role in DNA repair and apoptosis. [...] Read more.
Background: Triple-negative breast cancer (TNBC) is an aggressive subtype lacking estrogen, progesterone, and HER2 receptors, and is associated with poor prognosis and limited targeted therapeutic options. TP53 mutations occur in the majority of TNBC cases, disrupting p53’s role in DNA repair and apoptosis. Beyond gene regulation, p53 also influences calcium signalling through store-operated calcium entry (SOCE), a critical pathway for cell survival and death. However, the impact of different TP53 mutation types on calcium signalling remains unclear. Methods: Calcium channel gene expression was analysed using publicly available TNBC datasets. Calcium channel expression and SOCE activity were assessed in TNBC cell lines with different TP53 mutations using quantitative PCR and calcium imaging (Fura-2AM). Cell proliferation was measured using acid phosphatase assays, while apoptosis was evaluated through caspase 3/7 activation using the Incucyte live-cell fluorescent imager. The p53 reactivator COTI-2 was tested for its ability to restore TP53 function and modulate calcium signalling. Results: Analysis revealed significant downregulation of CACNA1D in TP53-mutant TNBCs. TNBC cell lines harbouring frameshift and stop TP53 mutations exhibited reduced SOCE, lower CACNA1D expression, and resistance to thapsigargin-induced apoptosis compared to wild-type cells. In contrast, cells with the TP53 R273H missense mutation demonstrated similar calcium signalling and proliferation to TP53 wild-type cels. COTI-2 treatment restored CACNA1D expression and SOCE in frameshift and stop mutant cells, enhancing apoptotic sensitivity. Combined treatment with COTI-2 and thapsigargin resulted in a synergistic increase in apoptosis. Conclusions: This study identifies a novel link between TP53 mutation type and calcium signalling in TNBC. Reactivating mutant p53 with COTI-2 restores calcium-mediated apoptosis, supporting combination strategies targeting both TP53 dysfunction and calcium signalling. Full article
(This article belongs to the Special Issue Calcium Signaling in Cancer Cell Progression)
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