目的观察全反式维甲酸(ATRA)对急性前髓性白血病细胞HL60生长的影响,探讨其抑制肿瘤生长的作用方式。方法建立急性前髓性白血病细胞HL60的裸鼠皮下实体瘤模型,经尾静脉隔日给予ATRA,第14天测量肿瘤大小;体外实验中,用免疫荧光法检测分化相关抗原CD11b的表达,观察ATRA对HL60分化水平的影响,用碘化丙啶(PI)染色法观察ATRA对HL60的细胞周期的影响。结果 ATRA治疗14 d后,ATRA组瘤体体积为(0.5±0.6)cm3,对照组为(1.9±1.7)cm3(P〈0.05);体外实验中,ATRA处理HL60细胞72 h后,细胞分化相关抗原CD11b的表达为(27.3±3.2)%,对照组(5.1±3.2)%(P〈0.01);ATRA处理HL60细胞24 h后,检测细胞周期分布比例,ATRA处理组静止期(G0/G1期)细胞比例为(57.6±1.5)%,对照组(43.0±2.0)%(P〈0.01)。结论 ATRA能够有效抑制HL60实体瘤的生长;体外实验证实,ATRA抑制HL60生长的作用机制是诱导细胞G0/G1期阻滞,诱导细胞分化。
Objective To study the influence of all-trans retinoic acid (ATRA) on acute promyelocytic leukemia cell line(HL60) differentiation and cell cycle distribution and determine the effective pattern by which ATRA inhibits tumor growth. Methods To create the HL60 cell line subcutaneous xenograft tumor model in nude mice, which were treated with ATRA through tail vain every other day and the volume of tumor was measured on day 14. In vitro, the expression of CD11 b, a differentiation marker,was detected by using immunofluorescence technique, and cell cycle was tested by PI stain assay. Results The volume of xenograft tumor was (0.5±0.6) cm3 in the ATRA group after 14 days" treatment, which was ( 1.9± 1.7 ) cm3 in the control group( P〈0.05 ). In vitro, the expression of differentiation marker CD11 b was (27.3±3.2 )% in the ATRA group and (5.1 ±3.2)% in the control group(P〈0.01 )after cultivation for 72 hours. Being co-cultured with ATRA for 24 hours, the cell cycle distribution of HL60 was analyzed, G0/G1 phase was ( 57.6 ± 1.5 ) % in the ATRA group and (43.0±2.0) % in the control group (P〈0.01). Conclusion The growth of xenograft tumor was inhibited by ATRA through tail vain injection,which may be associated with cell differentiation induction and cell cycle blockage.