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目的探讨激素抵抗性前列腺癌细胞增殖、凋亡状态和Caspase-3活性及意义。方法应用DNA电泳、流式细胞术(FCM)等技术检测了12例正常前列腺(NP)、31例激素性前列腺痛(HRPC)和31例激素依赖性前列腺癌(HDPC)组织DNA条带、DNA指数(DI)、增殖指数(PI)、细胞周期和Caspase-3活性,评价激素抵抗性前列腺癌组织增殖凋亡状况和Caspase-3活性。结果 HRPC DI、细胞异倍体率明显高于HDPC和NP组织,且G_1/G_0期细胞减少,S期和G_2/M期细胞增多(P<0.05),其中SPF明显升高(P<0.01)。NP、HRPC及HDPC组织前列腺癌组织G_1期前端均出现了一个称之为凋亡峰的亚倍体峰(亚G_1期),但HRPC细胞的凋亡峰明显低于HDPC和NP组织。HRPC组织细胞增殖指数(PI)明显高于HDPC和NP组织,HRPC凋亡峰值(AI)明显降低,PCa组织PI/AI明显增高,差异均有统计学意义(P<0.01)。NP、HRPC和HDPC组织Caspase-3均处于活性状态,但HRPC组织细胞内caspase-3活性明显低于HDPC和NP组织(P<0.01)。结论与HDPC相比,HRPC细胞表现为异倍体率增高、增殖过度和细胞凋亡减少,且呈现明显的增殖凋亡失衡状态。细胞凋亡Caspase家族的Caspase-3活性下降可能与HRPC发生和进展过程相关。
Objective To investigate the proliferation, apoptosis and Caspase-3 activity of hormone-resistant prostate cancer cells and its significance. Methods The DNA bands of 12 cases of normal prostate (NP), 31 cases of hormone-refractory prostatodynia (HRPC) and 31 cases of hormone-dependent prostate cancer (HDPC) were detected by DNA electrophoresis and flow cytometry (FCM) (DI), proliferative index (PI), cell cycle and Caspase-3 activity were measured to evaluate the proliferation and apoptosis status and Caspase-3 activity in hormone-resistant prostate cancer. Results Compared with HDPC and NP, HRPC DI was significantly higher than that in HDPC and NP tissues. The number of cells in G_1 / G_0 phase and the cells in S phase and G_2 / M phase increased (P <0.05), and SPF increased significantly (P <0.01) . A subpopulation peak (sub-G1 phase) appeared in the G_1stage of NP, HRPC and HDPC tissues, but the apoptotic peak of HRPC cells was significantly lower than that of HDPC and NP tissues. The cell proliferation index (PI) of HRPC was significantly higher than that of HDPC and NP. The peak of apoptosis (AI) of HRPC was significantly decreased and the PI / AI of PCa was significantly higher than that of HDPC (P <0.01). Caspase-3 in NP, HRPC and HDPC tissues were all active, but the activity of caspase-3 in HRPC tissues was significantly lower than that in HDPC and NP tissues (P <0.01). Conclusion Compared with HDPC, HRPC cells showed the increase of aneuploidy, hyperproliferation and decrease of apoptosis, and showed an imbalance of proliferation and apoptosis. Apoptotic Caspase family Caspase-3 activity decline may be associated with the occurrence and progression of HRPC.