Nuclear receptor coactivator-3 (NCOA3, SRC-3), a 1420-AA nuclear receptor coactivator, does not directly bind to DNA. It is recruited to specific gene promoters by interacting with nuclear hormone receptors such as the progesterone receptor, estrogen receptor, and peroxisome proliferation activated receptor and other transcription factors such as E2F1, PEA3, and AP1.

         It is reported that NCOA3 which is amplified in breast cancer 1 (AIB1) and also plays an important role in lung, ovary, prostate and pancreatic cancer over-expresses in many cancer cells. ^[1] NCOA3 plays an important role in optimal activation of the PERK–eIF2α–ATF4 pathway. XBP1–NCOA3 axis regulates cell fate decisions in ER-positive breast cancer cells. The PERK–ATF4 arm directly upregulated vascular endothelial growth factor A (VEGFA) and Lysosomal-Associated Membrane Protein 3 (LAMP3), thereby regulating tumour vascularity and invasion.^[2] Moreover, the phosphorylation of NCOA3 can further increase the transcriptional activity of NCOA3. So the phosphorylation of NCOA3 is also a biomarker for many cancers. ^[3]

          On April 3, 2018, a heavy study which was done by the team of Bert O'Malley at Baylor College of Medicine was published in the top journal "Nature". It revealed that PFKFB4 in glycolysis could even modify the phosphorylation of NCOA3, and thus became an accomplice to the proliferation and metastasis of breast cancer cells.^[4]

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