目的:探究乔松素(pinocembrin，Pin)对食管鳞癌细胞恶性进展的影响及对 Janus 酪氨酸激酶2(janus activated kinase 2，JAK2)/信号传导与转录激活子 3(signal transducer and activator of tran-scription 3，STAT3)信号通路的调控机制。方法:将人食管鳞癌细胞KYSE-410 随机分为KYSE-410 组、Pin低浓度(Pin-L)组、Pin中浓度(Pin-M)组、Pin 高浓度(Pin-H)组、Pin-H+JAK2 激活剂(Pin-H+ Broussonin E)组。采用CCK-8 法和克隆平板实验检测各组细胞的增殖活性;采用Transwell实验检测细胞的迁移和侵袭能力;采用流式细胞术检测各组细胞的凋亡情况;采用 Western blot 检测各组细胞中JAK2/STAT3 信号通路相关蛋白的表达水平。结果:与KYSE-410 组相比，Pin-L组、Pin-M组和Pin-H组细胞存活率(79。91±2。31、62。33±1。41、51。17±1。05，F=307。400)，克隆细胞形成数量(162。82±6。33、144。59±5。09、120。18±3。72，F=209。800)，迁移细胞数(77。73±3。26、60。83±2。41、49。28±1。60，F=360。314)，侵袭细胞数(62。72±2。42、50。93±2。07、32。47±1。55，F=460。221)以及细胞中 p-JAK2/JAK2(0。77±0。06、0。60±0。04、0。42±0。03，F=68。226)和 p-STAT3/STAT3 值(0。70±0。06、0。58±0。04、0。39±0。03，F=61。160)均降低(P<0。001)，而细胞凋亡率(24。72±2。18、39。62±3。66、48。33±4。13，F=235。118)升高(P<0。001)，Broussonin E的加入逆转了 Pin 对 KYSE-410 细胞恶性进展的抑制作用(P<0。05)。结论:Pin能够对食管鳞癌细胞的恶性进展起到抑制作用，其作用机制可能与 JAK2/STAT3 信号通路被抑制有关。
Pinocembrin Inhibits the Malignant Progression of Esophageal Squamous Carcinoma Cells via the JAK2/STAT3 Signaling Pathway
Objective:To investigate the effect of pinocembrin(Pin)on the malignant progression of e-sophageal squamous carcinoma cells and its regulatory mechanism on the Janus activated kinase 2(JAK2)/signal transducer and activator of transcription 3(STAT3)signaling pathway.Methods:Human esophageal squamous carcinoma cell line KYSE-410 was randomly separated into KYSE-410 group,Pin-low concentra-tion(Pin-L)group,Pin-medium concentration(Pin-M)group,Pin-high concentration(Pin-H)group,and Pin-H+JAK2 activator(Pin-H+Broussonin E)group.CCK-8 method and clone plate assay were ap-plied to detect the proliferative activity of cells in each group.Transwell experiment was applied to detect the migration and invasion abilities of cells;flow cytometry was applied to detect the apoptosis of cells in each group;Western blot was applied to detect the expression levels of JAK2/STAT3 signaling pathway related pro-teins of cells in each group.Results:Compared with the KYSE-410 group,the cell survival rates(79.91±2.31,62.33±1.41,51.17±1.05,F=307.400),the number of clone cells formed(162.82±6.33,144.59±5.09,120.18±3.72,F=209.800),and the number of migrated cells(77.73±3.26,60.83±2.41,49.28±1.60,F=360.314)were observed in the Pin-L,Pin-M,and Pin-H groups.The number of invasive cells(62.72±2.42,50.93±2.07,32.47±1.55,F=460.221),as well as p-JAK2/JAK2(0.77±0.06,0.60±0.04,0.42±0.03,F=68.226)and p-STAT3/STAT3 values(0.70±0.06,0.58±0.04,0.39±0.03,F=61.160)in the cells,decreased(P<0.001),while the apoptosis rate(24.72±2.18,39.62±3.66,48.33±4.13,F=235.11)increased(P<0.001),the addition of Broussonin E reversed the inhibitory effect of Pin on the malignant progression of KYSE-410 cells(P<0.05).Conclusion:Pin can inhibit the malignant progression of esophageal squamous carcinoma cells,and its mechanism of action may be related to the inhibi-tion of the JAK2/STAT3 signaling pathway.
PinocembrinJanus activated kinase 2Signal transducer and activator of transcrip-tion 3Esophageal squamous cell carcinoma
万方数据
维普
