Involvement of the JAK2/STAT5 Pathway in Human Prolactin Effects on Calcitonin Secretion by TT Cells

Chien-Chen Lu

《Adaptive Medicine》 Volume 13 (2021/09) Pp. 20-27

https://doi.org/10.4247/AM.2021.ACB260

Abstracts

Janus kinase 2 (JAK2) and signal transducer and activator of transcription 5 (STAT5) are involved in the effects of prolactin (PRL). PRL may stimulate thyroid gland calcitonin (CT) secretion. The mechanism by which PRL induces CT secretion, however, remains unclear. TT cells are derived from human medullary thyroid cancer and are parafollicular cells of the thyroid gland. TT cells were cultured in Nutrient Mixture F12 Ham Kaighn's Modification medium. After pre-incubation, the cells were challenged with a medium containing human PRL (hPRL) and JAK inhibitor I. The cells were disrupted at the end of the incubation. We measured the cellular levels of phosphorylated (p)-JAK2, JAK2, p-STAT5a, STAT5, ribosomal protein S6 kinase (p70-S6K), p-p70-S6K, and CT. hPRL increased cellular p-JAK2, JAK2, p-STAT5a, STAT5, p-p70-S6K, p70-S6K, and CT levels as well as the nuclear p-STAT5a level. Furthermore, the hPRL-induced effects were blocked by 50 nM JAK inhibitor I. In summary, our results suggest that the effects of hPRL on CT secretion in TT cells are mediated by JAK2, STAT5, and p70-S6K.

Keywords

calcitonin ； human prolactin ； p70-S6K ； human