Skip to main content
. Author manuscript; available in PMC: 2022 Nov 27.
Published in final edited form as: Cancer Lett. 2022 Feb 3;531:71–82. doi: 10.1016/j.canlet.2022.01.028

Fig. 3.

Fig. 3.

Androgen receptor (AR)-mediated regulation of prostate cancer. Directionality of the arrows (up = increase, down = decrease) and font color (red = increase, green = decrease) indicate the expression level of these drivers in Black men compared to White men with prostate cancer. Canonical AR signaling is mediated through androgen binding AR in the cytoplasm, which leads to a conformational change in AR causing it to dimerize. Upon dimerization, AR translocates to the nucleus and binds to androgen response elements (ARE) to allow transcription of many cancer-related genes. In Black men with prostate cancer, PSA and c-Myc levels are higher and TMPRSS2/ERG fusion rates are lower compared to White men with prostate cancer. A non-canonical AR signaling pathway mediated through PI3K and Akt also regulates AR signaling via phosphorylation. Many components of the PI3K pathway are upregulated in Black men with prostate cancer, including increased serum levels of growth factors, increased MNX1 activity, and preferential deletion of RGS12, leading to higher transcription of lipid metabolism genes such as SREBP1 and FASN.