Research Paper Volume 12, Issue 24 pp 24671—24692

Figure 6. A PR isoform-dependent cross-talk between prolactin and FASN in breast cancer: a working model. The convergence of prolactin/PRLR and PR signaling interactions on STAT5 [130, 131] might explain, at least in part, the PR-B-driven capacity of prolactin to activate FASN in luminal breast cancer cells (A). Similar inputs, likely involving yet-to-be explored phospho-modifications of PR isoforms, might underlie also the ability of FASN signaling to regulate autocrine prolactin secretion (B).