Manipulating calcium homeostasis with nanoplatforms for enhanced cancer therapy

This review paper provides a comprehensive overview of nanoplatforms that manipulate calcium ions (Ca2+) homeostasis to enhance cancer therapy. It offers a detailed exploration of two Ca2+ regulation strategies employed by these nanoplatforms, including Ca2+ overload and inhibition, and discusses the applications of Ca2+-related nanomaterials in various cell types, such as cancer cells and immune cells. The paper also presents perspectives on further advancing nanoplatforms for regulating Ca2+ homeostasis, identifying scientific limitations, and outlining future directions for exploration.


Calcium ions (Ca2+) are indispensable and versatile metal ions that play a pivotal role in regulating cell metabolism, encompassing cell survival, proliferation, migration, and gene expression. Aberrant Ca2+ levels are frequently linked to cell dysfunction and a variety of pathological conditions. Therefore, it is essential to maintain Ca2+ homeostasis to coordinate body function. Disrupting the balance of Ca2+ levels has emerged as a potential therapeutic strategy for various diseases, and there has been extensive research on integrating this approach into nanoplatforms. In this review, the current nanoplatforms that regulate Ca2+ homeostasis for cancer therapy are first discussed, including both direct and indirect approaches to manage Ca2+ overload or inhibit Ca2+ signalling. Then, the applications of these nanoplatforms in targeting different cells to regulate their Ca2+ homeostasis for achieving therapeutic effects in cancer treatment are systematically introduced, including tumour cells and immune cells. Finally, perspectives on the further development of nanoplatforms for regulating Ca2+ homeostasis, identifying scientific limitations and future directions for exploitation are offered.

Author list:

Yanlin Feng†, Jianlin Wang†, Jimin Cao*, Fangfang Cao*, Xiaoyuan Chen*

How to cite:

Y. Feng, J. Wang, J. Cao, F. Cao, X. Chen, Exploration 2023, 4, 20230019.