CAJ | 학술논문

目的探讨转化生长因子β1(TGF-β1)/SMAD信号通路在六亚甲基二乙酰胺(HMBA)抑制K562细胞增殖中的作用.方法采用HMBA诱导K562细胞分化模型后,四甲基偶氮唑盐(MTT)实验和流式细胞术分别检测HMBA对K562细胞的增殖和细胞周期作用,逆转录.聚合酶链反应(RT-PCR)检测TGF-β1、SMAD3、SMAD4和亲嗜性病毒整合位点1(EV11)在基因水平上相对表达量的变化趋势.结果 HMBA能抑制K562细胞增殖并促进其分化,作用程度随时间延长或剂量加大而增大,作用72 h时半数抑制浓度(IC50)为2 mmot/L.K562细胞经2 mmol/L HMBA作用72 h内,G0-G1期细胞百分率逐渐增高;TGF-β1、SMAD3和SMAD4在mRNA水平的相对表达量逐渐增高,而EVI1在mRNA水平的相对表达量逐渐降低.结论HMBA通过TGF-β1/SMAD信号通路抑制K562细胞增殖.
목적탐토전화생장인자β1(TGF-β1)/SMAD신호통로재륙아갑기이을선알(HMBA)억제K562세포증식중적작용.방법채용HMBA유도K562세포분화모형후,사갑기우담서염(MTT)실험화류식세포술분별검측HMBA대K562세포적증식화세포주기작용,역전록.취합매련반응(RT-PCR)검측TGF-β1、SMAD3、SMAD4화친기성병독정합위점1(EV11)재기인수평상상대표체량적변화추세.결과 HMBA능억제K562세포증식병촉진기분화,작용정도수시간연장혹제량가대이증대,작용72 h시반수억제농도(IC50)위2 mmot/L.K562세포경2 mmol/L HMBA작용72 h내,G0-G1기세포백분솔축점증고;TGF-β1、SMAD3화SMAD4재mRNA수평적상대표체량축점증고,이EVI1재mRNA수평적상대표체량축점강저.결론HMBA통과TGF-β1/SMAD신호통로억제K562세포증식.
Objective To investigate the effect of TGF-β1/SMAD signaling pathway on K562 cells growth inhibition caused by HMBA. Methods After establishing the in vitro differentiation model with HMBA on K562 cells, the MTT assay was used to detect the proliferation of K562 cells, the cell cycle profile was detected by flow cytometry, and the mRNA expression of TGF-β1, SMAD3, SMAD4 and EVI1 was measured by RT-PCR assay. Results HMBA could inhibit the proliferation and promote the differentiation of K562 cells obviously, which was time and concentration-dependent, and the 72 h corresponding IC50, was about 2 mmol/L. Within 72 h, flow cytometry assay indicated that the ration of G0-G1 phase cells was up-regulated, and the results of RT-PCR showed that relative mRNA expression of TGF-β1, SMAD3 and SMAD4 at mRNA level was increased gradually while that of EVI1 was decreased gradually. Conclusion HMBA can inhibit K562 cells proliferation through TGF-β1/SMAD signaling pathway.