Calcium Signaling in Cancer Cell Progression
A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".
Deadline for manuscript submissions: 31 March 2025 | Viewed by 41
Special Issue Editor
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
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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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