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目的 :通过化疗药物筛选富集胰腺癌干细胞,观察胰高血糖素样多肽-1(glucagon-like peptide-1,GLP-1)诱导胰腺癌干细胞的分化。方法 :应用0.05 mmol/L吉非替尼连续培养胰腺癌Panc-1细胞2周,筛选出吉非替尼耐药的S-Panc-1(selected Panc-1)细胞,并用10 nmol/L GLP-1处理72 h(命名为G-S-Panc-1细胞)。分别应用FCM法检测Panc-1、S-Panc-1和G-S-Panc-1细胞中CD133+细胞所占的比例,软琼脂克隆形成实验检测Panc-1和S-Panc-1细胞的克隆形成能力,裸鼠移植瘤实验检测S-Panc-1和G-S-Panc-1细胞的体内成瘤能力。结果 :S-Panc-1细胞中CD133+细胞所占比例[(55.5±1.7)%]明显高于Panc-1细胞[(1.7±0.2)%](P<0.01),G-S-Panc-1细胞中CD133+细胞所占比例明显下降(P<0.01),S-Panc-1细胞的体外克隆形成率[(1.20±0.16)%]明显高于Panc-1细胞[(0.31±0.02)%](P<0.01),G-S-Panc-1细胞裸鼠体内的成瘤能力明显低于S-Panc-1细胞(P<0.01)。结论 :吉非替尼耐药的Panc-1细胞具有肿瘤干细胞特征,GLP-1对胰腺癌干细胞可能具有诱导分化的作用。
OBJECTIVE: To screen and enrich pancreatic cancer stem cells by chemotherapeutic drugs and observe the differentiation of pancreatic cancer stem cells induced by glucagon-like peptide-1 (GLP-1). METHODS: Panc-1 pancreatic cancer cells were cultured continuously with 0.05 mmol / L gefitinib for 2 weeks. Gefitinib-resistant S-Panc-1 cells were screened and treated with 10 nmol / L GLP -1 for 72 h (named GS-Panc-1 cells). The proportion of CD133 + cells in Panc-1, S-Panc-1 and GS-Panc-1 cells was detected by FCM. The colony formation ability of Panc-1 and S-Panc- Nude mice xenografts were assayed for in vivo tumorigenicity in S-Panc-1 and GS-Panc-1 cells. Results: The percentage of CD133 + cells in S-Panc-1 cells was significantly higher than that in Panc-1 cells [(1.7 ± 0.2)%] (P <0.01) (55.5 ± 1.7% (1.20 ± 0.16)%] in S-Panc-1 cells was significantly higher than that in Panc-1 cells [(0.31 ± 0.02)%] (P < 0.01). The tumorigenicity of GS-Panc-1 cells in nude mice was significantly lower than that of S-Panc-1 cells (P <0.01). CONCLUSION: Gefitinib-resistant Panc-1 cells have tumor stem cell characteristics, and GLP-1 may induce differentiation of pancreatic cancer stem cells.