山东大学耳鼻喉眼学报 ›› 2025, Vol. 39 ›› Issue (1): 68-76.doi: 10.6040/j.issn.1673-3770.0.2024.154
• 论著 • 上一篇
张茂华1,魏日富1,朱忠寿1,刘平1,高尚1,2,李慧凤1
ZHANG Maohua1, WEI Rifu1, ZHU Zhongshou1, LIU Ping1, GAO Shang1,2, LI Huifeng1
摘要: 目的 探讨长链非编码RNA转录产物1(long non-coding RNA Prostate cancer associated transcript-1, lncRNA PCAT-1)对鼻咽癌HK-1细胞生物学行为及化疗敏感性的影响。 方法 实时定量 PCR(Real-time quantitative PCR, RT-qPCR)检测LncRNA PCAT-1在不同鼻咽癌细胞株中的表达,CCK8、transwell、流式细胞术检测过表达/干扰LncRNA PCAT-1的HK -1细胞增殖、迁移、侵袭、凋亡的变化,蛋白免疫印记(Western blot, WB)检测上皮间质转化(epithelial-mesenchymal transition, EMT)通路相关蛋白的表达,细胞增殖实验检测5-FU及DDP的半数抑制率( median inhibition concentration, IC50)变化。 结果 LncRNA PCAT-1在HK-1细胞株中表达升高。过表达LncRNA PCAT-1后,HK-1细胞的增殖、迁移、侵袭显著增加,而凋亡减少;E-cadherin蛋白表达水平显著降低,vimentin和N-cadherin蛋白表达水平显著升高;过表达后HK-1细胞对5-FU及DDP的IC50升高,细胞克隆数增加。干扰LncRNA PCAT-1后则相反,HK-1细胞增殖、迁移、侵袭显著降低,而凋亡增加;E-cadherin蛋白表达量显著升高,vimentin和N-cadherin蛋白表达水平显著降低;干扰后HK-1细胞对5-FU及DDP的IC50降低,细胞克隆数减少;差异均有显著性意义(P<0.05)。 结论 lncRNA PCAT-1通过EMT途径来调控鼻咽癌HK-1细胞的生物学行为,并降低细胞对5-FU和DDP的药物敏感性。
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