目的 研究NEK2(中心体相关激酶2)在前列腺癌和良性组织中的表达情况及其与前列腺癌预后的相关性。方法 运用qRT-PCR检测NEK2在前列腺癌和癌旁组织的表达差异,通过组织芯片免疫组化染色检测的方法检验NEK2在前列腺癌和癌旁组织的表达情况,最后使用Taylor的数据对NEK2进行生物信息学分析。结果 qRT-PCR检测NEK2在前列腺癌组织的表达显著高于癌旁组织(6.93±0.15 vs 5.38±0.4,t=6.25,P=0.003),组织芯片免疫组化结果显示NEK2在前列腺癌组织的表达显著高于癌旁组织(5.84±0.56 vs 4.27±0.49,t=5.38, P<0.001),结合Taylor公用数据库分析,NEK2高表达组患者术后的生化复发生存率减少( χ²=4.33,P=0.037),NEK2高表达组和低表达组在前列腺癌总体生存率上没有明显区别( χ²=0.27,P=0.605)。结论 NEK2参与前列腺癌的发生、发展进程,同前列腺癌发病进程密切相关,通过检测前列腺癌患者NEK2的表达情况,可早期预测生化复发的概率,能够作为判断前列腺癌预后的潜在生物学标志物。

Objective To investigate the expression of NEK2(NIMA-related kinase 2)in prostate cancer as well as benign prostatic hyperplasia,and the involvement of NEK2 in the prognosis of prostate caner(PCa). Methods The different expression of NEK2 in the tissue of prostate cancer and the adjacent benign tissues of prostate were measured by real-time quantitative reverse transcriptase-polymerase chain reaction (QRT-PCR) analysis and immunohositochemistry analysis,and then bioinformatically analyzed using the Taylor dataset. Results QRT-PCR showed that NEK2 was highly expressed in PCa than in the adjacent benign tissues (6.93±0.15 vs 5.38±0.4,t=6.25,P=0.003). Immunohositochemistry analysis showed the expression of NEK2 was higher in PCa than in the adjacent benign tissues(5.84±0.56 vs 4.27±0.49,t=5.38, P<0.001). Furthermore, the biochemical recurrence-free time of PCa patients in high NEK2 expression groups significantly reduced( χ²=4.33,P=0.037). The overall survival time of PCa patients was not correlated to NEK2 expression levels( χ²=0.27,P=0.605). Conclusion The above findings suggest that NEK2 is associated with production and development of PCa, and also critically connected with the process of PCa,which indicate that we can predict the probability of the biochemical recurrence-free time by detecting the expression of NEK2 in PCa patients,and NEK2 can also become a potential biomarker for PCa prognosis.

目的 研究前列腺癌细胞中miR-221的表达情况及其对癌细胞增殖的影响。方法 运用实时荧光定量PCR(qRT-PCR)检测miR-221在前列腺正常细胞株与前列腺癌细胞株中表达的差异情况,利用细胞转染构建miR-221过表达LNCaP和DU145细胞株,再通过CCK8细胞增殖实验检测细胞增殖情况的变化。结果 qRT-PCR检测细胞株发现miR-221在PC3、LNCaP和DU145三种前列腺癌细胞株中表达量均比前列腺正常细胞株PrEC低 (F=254.197,P<0.001),其中两两比较差异也均有统计学意义。细胞转染技术构建的miR-221过表达LNCaP和DU145细胞株,经qRT-PCR结果显示,miR-221在LNCaP和DU145细胞株中的表达水平明显升高(LNCaP,倍数变化=2.24,t=3.46,P<0.01;Du145,倍数变化=2.24,t=4.29,P<0.01)。细胞增殖实验结果显示,过表达了miR-221的LNCaP(P<0.001)和DU145(P<0.001)细胞生长速度慢于对照组。结论 实验证明miR-221表达过度能减慢前列腺癌细胞的增殖,miR-221有可能成为前列腺肿瘤治疗的生物学标志物。

Objective To investigate miR-221 expression in prostate cancer cells and its influence on prostate cancer cell proliferation. Methods miR-221 expressions in prostate normal cell lines and cancer cell lines were measured by qRT-PCR. Overexpression of the miR-221 in LNCaP and DU145 cell lines used by cell transfection. Effects of the depletion on cell proliferation were assessed in vitro with CCK8. Results qRT-PCR showed miR-221 was lower expressed in PC3, LNCaP and DU145 than in PrEC(F=254.197, P<0.001), in which pairwise comparison also had significant differences. qRT-PCR showed miR-221 expression rose significantly in LNCaP and DU145 cell lines whose miR-221 was overexpression with cell transfection(LNCaP, Fold Change=2.24,t=3.46,P<0.001;Du145, Fold Change=2.24,t=4.29,P<0.001). Cell proliferation assay showed that growth of LNCaP(P<0.001) and DU145(P<0.001) cells whose miR-221 was overexpression was slower than the control group. Conclusion This study demonstrates miR-221 overexpression can inhibited the proliferation of prostate cancer cells for the first time, it also suggests that miR-221 has the potential to serve as a biomarker for PCa therapy.