Slc8a1, also known as solute carrier family 8 member A1, encodes the sodium/calcium (Na+/Ca2+) exchanger NCX1 [3]. It plays a crucial role in regulating intracellular calcium levels, which is essential for various cellular functions such as muscle contraction, neurotransmitter release, and gene expression [3]. The function of Slc8a1 is closely related to multiple biological processes and is involved in various disease-related pathways.

In uveal melanoma, loss of LKB1-SIK2 module upregulates Slc8a1, promoting tumor cell proliferation and survival. Inhibition of Slc8a1 combined with a mitochondria-targeted antioxidant enhances cell death in LKB1-and SIK2-negative uveal melanoma cells [1].

In recurrent spontaneous abortion (RSA) and uterine corpus endometrial carcinoma (UCEC), Slc8a1 was identified as a hub gene. In vitro experiments showed that it promotes proliferation and inhibits apoptosis and calcium ion concentration in HTR-8/SVneo cells, suggesting it may be a prognostic biomarker and immunotherapy target [2].

In neonatal hypoxic-ischaemic encephalopathy, miR-214-3p, a direct target of Slc8a1, is down-regulated while Slc8a1 is up-regulated. Over-expression of miR-214-3p promotes neuronal proliferation and inhibits apoptosis [4].

In conclusion, Slc8a1 is essential for regulating intracellular calcium levels and is involved in multiple biological processes. Studies using gene-knockout models or analyzing its expression changes in diseases have revealed its role in cancer, RSA, and neonatal hypoxic-ischaemic encephalopathy. Understanding Slc8a1 can provide insights into the mechanisms of these diseases and potential therapeutic targets.