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Background:Prostate cancer (PC) is a worldwide health dilemma and initially is dependent upon androgen stimulation carried out by the androgen receptor (AR).Therapies which inhibit this androgen stimulation are successful until the tumour becomes non reliant upon androgen supply through aberrant AR signalling, thus relapse occurs.Investigating the co-repressors of the AR may provide an alternative avenue for androgen independent prostate cancer treatment.A known co-repressor, namely Prohibitin (PHB) has been previously identified to be down-regulated in metastatic PC when compared to healthy controls.