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目的 探讨前列腺癌发病的基质 上皮相互作用机制。 方法 体外培养前列腺基质细胞和前列腺癌 (Pca)细胞系PC 3。分别取已用于培养一种细胞的培养液作为另一种细胞的条件培养液 ,观察条件培养液对细胞增殖的影响。用双层软琼脂分析法混合培养前列腺基质细胞和PC 3细胞。用MTT法检测不同浓度TGFβ1对PC 3细胞增殖率的影响。用免疫组化SP法研究基质中平滑肌细胞的比例。用RT PCR方法检测基质细胞TGFβ1的表达。 结果 PC 3细胞的增殖在混合培养时受到抑制。混合培养 3周PC 3细胞的增殖率仅为隔离培养者的 6 2 % (P <0 .0 1)。条件培养液的PC 3细胞 48h细胞增殖率仅为无条件培养液对照组的 41% (P <0 .0 1)。PC 3细胞的增殖在加入TGFβ1后受到抑制 ,随TGFβ1浓度的增加 ,对PC 3细胞的抑制作用增强 ;随TGFβ1作用时间的延长 ,相同浓度的TGFβ1抑制效应更显著 (P <0 .0 1)。前列腺基质细胞表达大量的TGFβ1。 结论 前列腺基质细胞可以通过分泌TGFβ1抑制PC 3的增殖。前列腺癌的基质可能存在病变 ,使癌变的上皮逃脱基质的抑制作用
Objective To explore the mechanism of stromal epithelial interaction in the pathogenesis of prostate cancer. Methods Prostate stromal cells and prostate cancer (PCa) cell line PC 3 were cultured in vitro. The culture broth that has been used for culturing one kind of cells is separately taken as the conditioned broth of the other cells to observe the effect of the conditioned broth on the cell proliferation. Prostate stromal cells and PC 3 cells were mixed by double soft agar assay. The effect of different concentrations of TGFβ1 on the proliferation of PC 3 cells was detected by MTT assay. The proportion of smooth muscle cells in the stroma was examined by immunohistochemical SP method. The expression of TGFβ1 in stromal cells was detected by RT-PCR. Results Proliferation of PC 3 cells was inhibited during mixed culture. The proliferative rate of PC 3 cells in mixed culture for 3 weeks was only 62% (P <0.01) in isolated culture. Conditioned medium PC3 cells 48h cell proliferation rate was only 41% of the unconditional medium control group (P <0.01). The proliferation of PC 3 cells was inhibited after addition of TGFβ1, and the inhibitory effect on PC 3 cells increased with the increase of TGFβ1 concentration. With the prolongation of TGFβ1, the inhibitory effect of TGFβ1 at the same concentration was more significant (P <0.01) . Prostate stromal cells express large quantities of TGFβ1. Conclusion Prostate stromal cells can inhibit the proliferation of PC 3 by secreting TGFβ1. Prostate cancer may exist in the matrix of the lesion, so that cancerous epithelial escape matrix inhibition