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首页> 外文期刊>British Journal of Cancer >Castration plus oestrogen treatment induces but castration alone suppresses epithelial cell apoptosis in an androgen-sensitive rat prostatic adenocarcinoma
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Castration plus oestrogen treatment induces but castration alone suppresses epithelial cell apoptosis in an androgen-sensitive rat prostatic adenocarcinoma

机译：去势加雌激素治疗可诱导但单独去势可抑制雄激素敏感性大鼠前列腺腺癌中的上皮细胞凋亡

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The positive effect of castration in prostatic cancer patients is considered to be related to the induction of apoptosis in androgen-dependent tumour cells. However, castration apparently does not induce apoptosis in the highly differentiated, androgen-sensitive Dunning R3327PAP rat prostatic adenocarcinoma. To elucidate potential mechanisms of apoptotic induction in this tumour model, rats with subcutaneously implanted tumours were treated with vehicle (I), castration+vehicle (C) or castration + 50 micrograms of oestradiol benzoate per day s.c. (C + E2). The effects on tumours were examined by morphometry, in situ end labelling (ISEL) of apoptotic cells and immunohistochemically with monoclonal antibodies to proliferating cell nuclear antigen (PCNA) at different time points up to 168 h after castration. Castration inhibited tumour growth and decreased the epithelial cell apoptotic rate (from 12 h) and epithelial cell proliferation rate (from 72 h) compared with that in the I group. Tumour volume, volume densities of epithelium and stroma and stroma cell proliferation rate remained constant in the C group during the study period. C + E2 treatment resulted in increases in cell proliferation in the stroma (from 12 h) and in the volume density of stroma (from 24 h) compared with that in the C and I groups. The number of apoptotic epithelial cells was increased (from 24 h), and this was followed by decreases in the volume density of epithelium (from 24 h), the epithelial cell proliferation rate (from 72 h) and the total tumour volume (from 72 h). We conclude that in the Dunning R3327PAP tumour model C + E2 treatment is more effective than castration alone. C+E2 treatment, in contrast to C, is able to induce tumour cell death and to decrease total tumour volume. The mechanism behind this effect is unknown, but it could be related to stimulatory effects of E2 in the tumour stroma.
机译：前列腺癌患者去势的积极作用被认为与雄激素依赖性肿瘤细胞凋亡的诱导有关。但是，去势显然不会诱导高度分化的雄激素敏感性Dunning R3327PAP大鼠前列腺腺癌中的细胞凋亡。为了阐明在该肿瘤模型中凋亡诱导的潜在机制，每天皮下用媒介物（I），去势+载体（C）或去势+50微克雌二醇苯甲酸酯处理皮下植入的肿瘤的大鼠。 （C + E2）。通过形态计量学，凋亡细胞的原位末端标记（ISEL）并在去势后直至168 h的不同时间点用抗增殖细胞核抗原（PCNA）的单克隆抗体免疫组化检查对肿瘤的影响。与I组相比，去势抑制了肿瘤的生长，降低了上皮细胞的凋亡率（从12 h开始）和上皮细胞的增殖速率（从72 h开始）。在研究期间，C组的肿瘤体积，上皮和间质的体积密度以及间质细胞增殖率保持恒定。与C组和I组相比，C + E2处理导致基质细胞增殖（从12 h开始）和基质体积密度（从24 h开始）增加。凋亡的上皮细胞数量增加（从24小时开始），随后是上皮的体积密度（从24小时开始），上皮细胞增殖速率（从72小时开始）和总肿瘤体积（从72小时开始）降低H）。我们得出的结论是，在Dunning R3327PAP肿瘤模型中，C + E2治疗比单独去势更为有效。与C相反，C + E2治疗能够诱导肿瘤细胞死亡并减少总肿瘤体积。这种作用背后的机制尚不清楚，但可能与E2对肿瘤基质的刺激作用有关。

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