# Store-Operated Calcium Entry As an Important Mechanism of Tumor Adaptation to an Aggressive Microenvironment

## TL;DR

This paper explores how calcium signaling, specifically store-operated calcium entry, helps cancer cells adapt to harsh conditions in the tumor microenvironment.

## Contribution

The paper highlights the role of calcium signaling remodeling as a potential adaptation mechanism in aggressive tumor environments.

## Key findings

- Tumor cells show altered expression of proteins involved in store-operated calcium entry.
- Microenvironmental factors like acidification and hypoxia affect calcium channel function.
- Understanding these changes may reveal whether they are adaptive or due to cancer development.

## Abstract

Calcium signaling ensures efficient cellular functioning; calcium homeostasis
disruption leaves behind detrimental sequelae for the cell both under calcium
excess and deficiency conditions. Malignant transformation is accompanied by
significant alterations in the expression of the proteins critical for
store-operated calcium entry, resulting in the dysregulation of calcium
signaling. It is plausible that a remodeling of intracellular signal
transduction pathways in cancer cells is required in order to accelerate
metabolic processes, as well as fuel further tumor growth and invasion.
Meanwhile, fine-tuning of calcium signaling is observed under both normal and
pathological conditions. In this context, research into the changes
accompanying signal transduction within the tumor microenvironment is a key
aspect of the investigation of the role of calcium signaling in tumor
development. Factors characteristic of the tumor microenvironment were shown to
have a significant effect on the function of calcium channels and the proteins
that regulate calcium signaling. Major, adverse microenvironmental factors,
such as acidification, elevated levels of reactive oxygen species and hypoxia,
have a bearing on the store-operated calcium entry. It is crucial to understand
whether changes in the expression of the key SOCE components represent an
adaptation to the microenvironment or a result of carcinogenesis.