Calcium Signaling and Its Dysregulation in Cancer
A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".
Deadline for manuscript submissions: closed (15 July 2022) | Viewed by 17937
Special Issue Editor
Interests: epithelial differentiation processes in breast, oral, and lung cancers; metastasis mechanisms; cell junctional signaling; EGFR, Her2, and E-cadherin in anoikis; role of intracellular calcium stores in proliferation, differentiation, and cell death; p53, cell stress, and DNA damage response; cell senescence; CLCA gene family
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Special Issue Information
Dear Colleagues,
There is a growing appreciation of the role that intracellular calcium plays in both tumor suppression and progression. Calcium is the common currency of differentiation and homeostasis. It is stored primarily in the endoplasmic reticulum, rationed according to need, and replenished from the extracellular milieu via store-operated calcium entry (SOCE). This currency is disbursed by the inositol triphosphate (IP3) receptor in response to diverse extracellular signals. The rate of release is governed by regulators of metabolism and proliferation, differentiation, autophagy, survival, and programmed cell death, with different outcomes depending on the strength of the signal and context. This system is fundamentally tumor-suppressive, and cancer cells must find ways to subvert it in order to exploit its growth-promoting effects.
This Special Issue invites both original manuscripts describing novel findings and cutting-edge review articles illustrating the many mechanisms by which cancer cells dysregulate SOCE, IP3 and ryanodine receptors, calcium transfer to mitochondria, and signaling to downstream effectors and targets to prevent cell death and enhance metabolism, mitogenesis, and metastasis.
Prof. Dr. Randolph C. Elble
Guest Editor
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Keywords
- intracellular calcium
- IP3R
- SOCE
- RyR
- STIM
- ORAI
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