Fig. 2.

Advances of the STAT3 signaling pathways involved in breast cancer progression. Interleukins, including IL-6, IL-8 and IL-35, can bind to their receptors and activate the phosphorylation of JAKs and STAT3, OSM can increase IL-6-mediated activation, and IL-17 binding to its receptor leads to inhibition of STAT3 phosphorylation. STAT3 phosphorylated by EGF can be inhibited by PTPN2. COX2 and prostaglandin E2 upregulated by HDAC6 can activate STAT3 phosphorylation, and SMYD2 has a similar effect. Additionally, STAT3 and NEAT1 can form a loop to activate the phosphorylation of STAT3, which is inhibited by miR-124. The activated and phosphorylated STAT3 dimers translocate into the nucleus and activate the transcription of target genes involved in breast cancer progression