Ligand-independent activation of the androgen receptor in prostate cancer by growth factors and cytokines.
During the course of prostate cancer progression, cells convert from an androgen-dependent to an androgen-independent growth status. At this late stage, the role of the androgens testosterone and dihydrotestosterone and their nuclear receptor, the androgen receptor (AR), is unclear. Has the growth pathway, initiated by the AR, been bypassed in androgen-independent tumours? Mounting evidence suggests the opposite. Prostate cancer cells that have acquired the ability to survive and grow in a low androgen environment might be activating the AR pathway using growth factors, cytokines, and steroids other than androgens.
Jenster
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D016207:Cytokines / Q000502:physiology*; D018450:Disease Progression; D006133:Growth Substances / Q000502:physiology; D006801:Humans; D008024:Ligands; D008297:Male; D009363:Neoplasm Proteins / Q000502:physiology*; D009376:Neoplasms, Hormone-Dependent / Q000378:metabolism; D011471:Prostatic Neoplasms / Q000378:metabolism* / Q000473:pathology; D011944:Receptors, Androgen / Q000378:metabolism*
D016207:Cytokines; D006133:Growth Substances; D008024:Ligands; D009363:Neoplasm Proteins; D011944:Receptors, Androgen