CAJ | 학술논문

目的：探讨雄激素受体（AR）在前列腺癌细胞系LNCaP中分选出的干/祖（S/P）细胞和非干/祖（non S/P）细胞的不同作用。方法采用流式细胞术从LNCaP中分选出S/P细胞和Non S/P细胞，使用慢病毒载体携带AR转入两种细胞，在不同的雄激素浓度（1 nmol/L和10 nmol/L）培养条件下，应用四甲基偶氮唑盐（MTT）实验，前列腺细胞球体形成实验，琼脂糖凝胶克隆形成实验，细胞迁移实验来比较AR在两种细胞中的不同作用。结果 AR转入S/P细胞，细胞生长受到抑制（P＜0.05），形成前列腺球的能力下降（P＜0.05），成瘤能力减弱（P＜0.05），细胞迁移能力下降（P＜0.05）；反之，AR转入non S/P细胞，细胞生长能力增强（P＜0.05），成瘤能力加强（P＜0.05），细胞迁移能力增强（P＜0.05）。结论 AR在前列腺癌细胞系LNCaP中分选出的S/P和non S/P细胞表达不同，发挥相反作用，这可能是现有前列腺癌内分泌治疗失败的原因之一。
목적：탐토웅격소수체（AR）재전렬선암세포계LNCaP중분선출적간/조（S/P）세포화비간/조（non S/P）세포적불동작용。방법채용류식세포술종LNCaP중분선출S/P세포화Non S/P세포，사용만병독재체휴대AR전입량충세포，재불동적웅격소농도（1 nmol/L화10 nmol/L）배양조건하，응용사갑기우담서염（MTT）실험，전렬선세포구체형성실험，경지당응효극륭형성실험，세포천이실험래비교AR재량충세포중적불동작용。결과 AR전입S/P세포，세포생장수도억제（P＜0.05），형성전렬선구적능력하강（P＜0.05），성류능력감약（P＜0.05），세포천이능력하강（P＜0.05）；반지，AR전입non S/P세포，세포생장능력증강（P＜0.05），성류능력가강（P＜0.05），세포천이능력증강（P＜0.05）。결론 AR재전렬선암세포계LNCaP중분선출적S/P화non S/P세포표체불동，발휘상반작용，저가능시현유전렬선암내분비치료실패적원인지일。
Objective Imploring the different role of androgen receptor(AR)in the stem/progenitor(S/P) cells and none stem/progenitor(non S/P) cells isolated from human prostate cancer cell line LNCaP. Methods The S/P and non S/P cells could be obtained through florescence-activated cell sorting (FACS). AR was transferred in S/P and non S/P cells with lentivirus vector. The role of AR in the two kinds of cells were compared in different experiments, such as MTT assay, prostate sphere formation assay, soft agar assay, cell immigration assay. Results After AR transfected in S/P cells, the cell growth was inhibited (P<0.05), the ability to form prostate sphere, the tumorigenesis ability, the capability of cell immigration all decreased (P<0.05), but in non S/P cells AR played a contrary role. AR promoted the cell growth (P<0.05). The tumorigenesis ability and the capability of cell immigration all increased(P<0.05). Conclusions AR play a contrary role in S/P and non S/P cells isolated from human prostate cancer cell line LNCaP. This may be one of the reasons for the failure of prostate cancer endocrine therapy.