OXER1 mediates testosterone-induced calcium responses in prostate cancer cells

In prostate cancer, calcium homeostasis plays a significant role in the disease's development and progression. Intracellular calcium changes are an important secondary signal, triggered by a variety of extracellular stimuli, that controls many cellular functions. One of the main events affecting calcium is androgen signaling. Indeed, via calcium changes, androgens regulate cell processes like cell growth, differentiation and motility. In the present work we explored the nature of the receptor involved in calcium response induced by membrane-acting testosterone in prostate cancer cells. We report that testosterone, independently of the presence of the classical androgen receptor, can rapidly increase intracellular calcium from calcium stores, through the oxoeicosanoid receptor 1 (OXER1) and a specific signaling cascade that triggers calcium release from the endoplasmic reticulum. These findings reveal for the first time the receptor involved in the rapid calcium changes induced by androgens. Moreover, they further support the notion that androgens, even in the absence of AR, can still exert specific effects that regulate cancer cell fate.

Automated summary

Calcium homeostasis plays a significant role in the development and progression of prostate cancer, with androgens regulating cell processes through calcium changes. The study found that testosterone can rapidly increase intracellular calcium levels through OXER1 receptor and specific signaling cascade. These findings reveal the receptor involved in rapid calcium changes induced by androgens in prostate cancer cells.