Heer R
Department of Urology, Freeman Hospital, High Heaton, Newcastle upon Tyne, NE7 7DN, UK.
Ann R Coll Surg Engl. 2011 Sep;93(6):424-8. doi: 10.1308/10.1308/147870811x589245.
A stem cell model of prostate cancer tumourigenesis explains progression to castration resistant prostate cancer (CRPC) and offers novel perspectives in targeting this cancer in its more advanced forms. Androgen receptor (AR) regulated pathways are central mechanisms in progression to CRPC. However, AR was thought to be lacking in prostate stem cell enriched fractions. Potential low levels of AR expression in stem cell enriched cells were investigated and potential direct effects of androgen were examined.
Human prostate stem cell enriched populations, based on high α(2)β(1) integrin expression (α(2)β(1)(hi)), were selected from primary human prostate tissue in men undergoing transurethral prostatectomy or cystoprostatectomy. Effects on differentiation were assayed with flow cytometry using differentiation-specific markers.
Low levels of AR were demonstrable in α(2)β(1)(hi) cells following inhibition of the proteasome using MG132. Furthermore, a direct effect of androgen was shown in stabilising/inducing AR expression. Androgen treatment of α(2)β(1)(hi) cells was associated with the induction of differentiation using a number of differentiation-specific markers (prostatic acid phosphatase, cytokeratin 18 and AR) with increases ranging from 49% to 67% (p<0.05). These effects were blocked with the AR-specific inhibitor bicalutamide (p<0.05). These data support a role of direct androgen activity on stem cell enriched cells in the prostate and the implications of these findings are discussed.
前列腺癌肿瘤发生的干细胞模型解释了其向去势抵抗性前列腺癌(CRPC)的进展,并为靶向治疗这种更晚期形式的癌症提供了新的视角。雄激素受体(AR)调节的信号通路是CRPC进展的核心机制。然而,人们认为前列腺干细胞富集组分中缺乏AR。本研究调查了干细胞富集细胞中潜在的低水平AR表达,并检测了雄激素的潜在直接作用。
从接受经尿道前列腺切除术或膀胱前列腺切除术的男性的原发性前列腺组织中,筛选出基于高α(2)β(1)整合素表达(α(2)β(1)(hi))的人前列腺干细胞富集群体。使用分化特异性标志物,通过流式细胞术检测对分化的影响。
使用MG132抑制蛋白酶体后,在α(2)β(1)(hi)细胞中可检测到低水平的AR。此外,雄激素在稳定/诱导AR表达方面具有直接作用。用多种分化特异性标志物(前列腺酸性磷酸酶、细胞角蛋白18和AR)检测发现,雄激素处理α(2)β(1)(hi)细胞与诱导分化相关,增加幅度在49%至67%之间(p<0.05)。这些作用被AR特异性抑制剂比卡鲁胺阻断(p<0.05)。这些数据支持雄激素对前列腺干细胞富集细胞具有直接活性的作用,并对这些发现的意义进行了讨论。