STAT transmit signals from extracellular polypeptides, through transmembrane receptors, directly to target gene promoters in the nucleus resulting in genetic reprogramming of the target cell.
STAT proteins are latent transcripton factors activated by tyrosine phosphorylation following recruitment to ligand activated receptor complexes.
There are 7 STAT space members, STAT1,2,3,5,5A,5B and 6.
All of the STAT members need to be phosphorylated on one or more sites to dimerize and the activity but translocated nucleus and induce transcription.
The JAK-STAT pathway when inhibited can lead to embryonic lethal phenotypes.
Tyrosine phosphorylation allows dimerization and accumulation within the nucleus.
STAT5 and STAT3 are clustered on chromosome 17q.
Activated STAT3 and STAT5 contributes to oncogenesis by stimulating proliferation and preventing a pop ptosis in various malignant diseases.
STAT proteins binding is increased in the nuclei of breast cancer patients compared with normal tissue or benign lesions.
STAT5 nuclear localizatio/phosphorylation is associated with improved survival in breast cancer.
STAT5 positive breast cancers may have an improved response with endocrine therapy.
STAT5 is an independent marker of outcome in patients with lymph node negative breast cancer, reduced expression associated with a 2.5 fold increase in the risk of recurrence and 2.4 fold risk of dying of breast cancer (Peck AR et al).
STAT5 nuclear levels decreases as the disease progresses from normal to in-siyu, to invasive and then to nodal metastases (Peck AR et al).
STAT5 Since in tumors of patients treated with anti-estrogen therapy is associated with poor breast cancer survival and nearly a seven fold increase in risk of dying from breast cancer despite anti-estrogen therapy But(Peck AR et al).