Fig. 3

Advances of the STAT3 signaling pathways involving breast cancer proliferation and apoptosis. Classical IL-6 /JAK/STAT3 pathways can activate the transcription of cyclin D-1, c-myc, bcl-2 and Bax to promote the proliferation and inhibit the apoptosis of breast cancer. miR-125a, miR-25-3p and p16 can promote the binding of IL-6 to its receptors, whereas Wwox has the opposite effect. CCL-18 binding to its receptor can activate the phosphorylation of STAT3, which can be inhibited by IL-32θ. The circuit loop of phosphorylated STAT3, TMEM16A and EGF leads to continuous activation of STAT3. miR-93-5p, SMYD2, TRIM14 and PKT-M2 induce the activation of STAT3, whereas miR-124 and miR-9 inhibit the activation of STAT3 and breast cancer proliferation. Let-7a-5p, hnRN-A and phosphorylated STAT3 dimers form a circuit loop to upregulate PKM2 and promote the proliferation and inhibit the apoptosis of breast cancer cells. DPF3 suppressed by phosphorylated STAT3 can promote breast cancer proliferation. Additionally, transcription factor EB (TFEB) can combine with phosphorylated STAT3 dimers to promote the transcription of target genes involved in breast cancer proliferation