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Calcium-Linked Messaging in Cancer

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

Deadline for manuscript submissions: closed (30 June 2026) | Viewed by 494

Editor

Special Issue Information

Dear Colleagues,

It is well established that cancer cells exhibit modified calcium signaling that facilitates several pro-tumoral processes, including proliferation, angiogenesis, exosome release, invasion, loss of death pathways, and response to chemotherapy. Consequently, the impairment of Ca2+ homeostasis is considered a crucial driver of cancer initiation and progression. Accumulating evidence indicates that the alterations of intracellular Ca2+ flux arise from aberrant expression or function of cation channels, pumps, sensors, and transporters, which, therefore, represent attractive targets for the development of innovative anticancer drugs.

Recently, interorganellar Ca2+ communication has gained considerable attention. 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 gather current knowledge on on the role of Ca2+ signaling in cancer, with a focus on the following:

- Membrane contact sites between mitochondria and endoplasmic reticulum or lysosomes;

- Interorganelle platforms connecting endosomes and the plasma membrane;

- Interorganelle Ca2+ flux and its impact on cancer cell metabolism and fate;

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

- Mitoflash and tumor progression;

- Ca2+ interplay between organelles and the exosome release.

Dr. Amantini Consuelo
Guest Editor

Manuscript Submission Information

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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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Review

43 pages, 2514 KB  
Review
Targeting Plasma Membrane Ca2+-ATPases in Cancer: Current Insights and Future Perspectives
by Malwina Lisek, Julia Tomczak, Natalia Bochenska, Julia Duraj and Tomasz Boczek
Cancers 2026, 18(15), 2450; https://doi.org/10.3390/cancers18152450 - 30 Jul 2026
Abstract
Calcium signaling is a fundamental regulator of cell physiology, controlling proliferation, differentiation, migration, metabolism, gene expression, and cell death. In cancer, these signaling pathways are extensively remodeled to generate spatially and temporally restricted Ca2+ signals that support malignant progression while avoiding calcium-induced [...] Read more.
Calcium signaling is a fundamental regulator of cell physiology, controlling proliferation, differentiation, migration, metabolism, gene expression, and cell death. In cancer, these signaling pathways are extensively remodeled to generate spatially and temporally restricted Ca2+ signals that support malignant progression while avoiding calcium-induced cytotoxicity. PMCAs traditionally regarded as high-affinity calcium extrusion pumps, have recently emerged as multifunctional regulators of compartmentalized calcium signaling. In addition to maintaining low cytosolic Ca2+ concentrations, PMCA isoforms organize specialized signaling microdomains by interacting with receptors, ion channels, scaffold proteins, and downstream signaling molecules, thereby selectively modulating calcium-dependent pathways involved in tumor growth and metastasis. Accumulating evidence demonstrates that PMCA isoforms exert distinct, context-dependent functions in cancer. PMCA1 primarily contributes to basal calcium homeostasis but has also been implicated in tumor progression, angiogenesis, and regulation of the tumor immune microenvironment. PMCA2 promotes survival and oncogenic signaling in HER2-positive breast cancer through stabilization of receptor signaling complexes. PMCA3 has been linked mainly to endocrine tumors and selected malignancies, although mechanistic evidence remains limited. PMCA4 exhibits the greatest functional diversity, acting either as a tumor suppressor or a promoter depending on the cancer type by regulating localized calcium signaling, cell migration, invasion, differentiation, and interactions with oncogenic signaling networks. This review summarizes current advances in the structural biology, regulation, and signaling functions of PMCA isoforms, with particular emphasis on their emerging roles in cancer biology. We also discuss the potential of PMCAs as prognostic biomarkers and therapeutic targets, highlighting the importance of isoform-specific strategies for targeting calcium signaling in cancer. Full article
(This article belongs to the Special Issue Calcium-Linked Messaging in Cancer)
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