论文部分内容阅读
目的 探讨前列腺癌组织中前列腺特异性同源框基因NKX3.1及抑癌基因PTEN(MMAC1/TEP1)蛋白的表达 ,相关性及意义 ;NKX3.1对其表达缺失株前列腺癌PC3细胞生长的影响效应。方法 对 30例前列腺腺癌 ,1例前列腺肉瘤 ,10良性前列腺增生 (BPH)进行组织NKX3.1与PTEN蛋白表达的免疫组化研究 ;稳定转染PC3细胞 ,研究NKX3.1对PC3细胞形态、细胞周期、增殖速率等影响。结果 (1) 31例前列腺恶性肿瘤组织NKX3.1蛋白阳性表达率 4 8.39% ,PTEN蛋白阳性表达率 2 9.0 3,良性前列腺增生中分别为 70 %、5 0 % ;未发现NKX3.1蛋白表达强度与PTEN蛋白表达存在相关性 ;(2 )稳定转染NKX3.1基因的PC3细胞形态明显改变 ,细胞从G1期到S期发生抑制 ,MTT检测示细胞增殖活性明显降低。提示转染外源性NKX3.1基因可阻滞PC3细胞由G1期进入S期 ,并抑制肿瘤细胞增殖。结论 NKX3.1与PTEN基因失活在前列腺肿瘤发病中有重要作用 ,NKX3.1对其表达缺失的雄激素非依赖性细胞株PC3有生长抑制效应
Objective To investigate the expression, correlation and significance of prostate cancer-specific homeobox gene (NKX3.1) and tumor suppressor gene PTEN (MMAC1 / TEP1) in prostate cancer tissue and the effect of NKX3.1 on the growth of prostate cancer PC3 cells effect. Methods Immunohistochemical study on the expression of NKX3.1 and PTEN in 30 cases of prostatic adenocarcinoma, 1 case of prostate sarcoma and 10 cases of benign prostatic hyperplasia (BPH) were performed. Stably transfected into PC3 cells, the effects of NKX3.1 on the morphology, Cell cycle, proliferation rate and other effects. Results (1) The positive expression rate of NKX3.1 protein in 31 cases of prostate cancer was 4 8.39%, the positive rate of PTEN protein was 2 9.0 3, and 70%, 50% in benign prostatic hyperplasia respectively. No expression of NKX3.1 protein was found (2) The morphology of PC3 cells stably transfected with NKX3.1 gene was significantly changed, and the cells were inhibited from G1 phase to S phase. The MTT assay showed that the cell proliferation activity was significantly decreased. It suggested that transfection of exogenous NKX3.1 gene could block PC3 cells from G1 phase into S phase and inhibit tumor cell proliferation. Conclusion NKX3.1 and PTEN gene inactivation plays an important role in the pathogenesis of prostate cancer. NKX3.1 inhibits the growth of PC3, an androgen-independent cell line,