摘要
目的探究二氢杨梅素(DHM)通过抑制ADAM 17对乳腺癌细胞MCF-7增殖和凋亡的影响及其发生机制。方法采用DHM对人乳腺癌MCF-7细胞进行干预,MTS分析细胞的增殖抑制率,流式细胞仪分析细胞的凋亡率,Western blot检测干预后细胞内ADAM17、JAK2和STAT3的表达。结果 40 nmol·L^(-1) DHM可显著抑制MCF-7细胞的增殖(P<0.05),干预24 h、48 h、72 h后,细胞增殖抑制率分别为(19.72±2.23)%、(69.35±2.41)%、(87.29±2.92)%,组间差异有统计学意义(P<0.05)。40 nmol·L^(-1) DHM可显著促进MCF-7细胞凋亡(P<0.05),干预24 h、48 h、72 h后,细胞凋亡率分别为(5.02±0.13)%、(9.37±0.21)%、(13.25±0.33)%,组间差异有统计学意义(P<0.05);40 nmol·L^(-1) DHM干预后,细胞内ADAM17、JAK2和STAT3表达水平显著降低(P<0.05)。结论 DHM可有效抑制乳腺癌细胞MCF-7增殖并促进其凋亡,其机制与下调ADAM17、JAK2和STAT3的表达相关。
Objective To explore the effects of dihydromyrieetin （DHM） on the proliferation of breast cancer MCF-7 cells through in- hibiting the expression of ADAM 17 and its mechanisms. Methods Human breast cancer MCF-7 cells were cultured and intervened with dihydromyrieetin. MTS was used to analyze the inhibition rate of the cells. The flow eytometl7 was applied to analyze the rate of cell apopto- sis. Western blot was used to detect the expression of ADAM17, JAK2 and STAT3 in the cells after intervention. Results The administration of 40 nmol.U1 DHM eould effeetively inhibit the proliferation rate of MCF-7 cells （P 〈 0.05）. The inhibition rate of eells inereased gradually after intervention, and it was （19.72 ± 2.23）% at 24 h, （69.35 ± 2.41）% at 48 h, and （87.29 ± 2.92）% at 72 h. There was a signifieant dif- ferenee in inhibition rate between the groups （P 〈 0.05）. Apoptosis results showed that administration of 40 nmol.U1 DHM significantly in- creased the apoptotie rate of MCF-7 cells （P 〈 0.05）. The apoptotie rate of cells increased gradually at 24 h, 48 h and 72 h after intervention, and was respeetively （5.02 ± 0.13） %, （9.37 ± 0.21） % and （13.25 ± 0.33） %, having a signifieant differenee between the groups （P〈0.05）. Western blot results showed that the expressions of ADAM17, JAK2 and STAT3 in MCF-7 cells were significantly decreased after interven- tion of 40 nmol.U＇ DHM （P 〈 0.05）. Conclusion DHM can inhibit the proliferation of breast cancer cell MCF-7 and promote its apoptosis effectively, and its mechanism is closely related to the down-regulation of ADAM17, JAK2 and STAT3 expression levels.
作者
李杨
戴雪明
王晔
茅届齐
尤天庚
L;DA;WANG Ye：;MAOJieqi;YOU Tiangeng(Department of General Surgery,Shanghai General Hospital,Shanghai Jiao Tong University School of Medicine Shanghai,200080,China;Department of Laparoscopic Surgery,Eastern HepatobiliaU SurgeU Hospital,Second Mili-taU Medical University,Shanghai,200438,China)
出处
《肿瘤药学》
CAS
2018年第4期528-530,554,共4页
Anti-Tumor Pharmacy
基金
上海市自然科学基金资助项目(16ZR1428200)
