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首页> 美国卫生研究院文献>Oncology Letters >Establishment and characterization of the gemcitabine-resistant human pancreatic cancer cell line SW1990/gemcitabine
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Establishment and characterization of the gemcitabine-resistant human pancreatic cancer cell line SW1990/gemcitabine

机译：耐吉西他滨的人胰腺癌细胞株SW1990 /吉西他滨的建立与表征

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Due to its rapid progression, metastasis and resistance to chemotherapy, pancreatic cancer is one of the most malignant tumor types to affect the digestive system. Gemcitabine chemotherapy is typically the first choice of treatment for advanced pancreatic cancer; however, chemoresistance is a major obstacle to successful treatment. In order to elucidate the underlying mechanisms of gemcitabine resistance in pancreatic cancer, the drug-resistant cell line SW1990-gemcitabine (SW1990-GZ) was established using the human pancreatic cancer cell line SW1990. The IC50, resistance index and growth of SW1990 and SW1990-GZ cells were also assessed using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assays. The cellular uptake of gemcitabine in SW1990 and SW1990-GZ was measured using high performance liquid chromatography (HPLC). The protein expression of p53 was also assessed by western blot analysis. The results demonstrated that the IC50 of SW1990 and SW1990-Gz was 0.07±0.0021 and 87.5±3.24 µg/ml, respectively, and that the resistance index ratio of SW1990-Gz was 1,250. The growth rate of SW1990-GZ cells was low compared with that of SW1990 cells. The HPLC results indicated that gemcitabine uptake was markedly reduced in SW1990-GZ cells compared with in SW1990 cells at different time points. The protein expression of p53 was significantly higher in GEM-resistant SW1990-GZ cells compared with that in SW1990 cells (P<0.01). These results suggest that a human gemcitabine-resistant pancreatic cancer cell line was successfully established, with stable and significant drug resistance. The results of the present study suggest that the decreased cellular uptake of gemcitabine may serve an important role in gemcitabine chemoresistance in SW1990-GZ cells; thus, this cell line may be used as an effective in vitro model to improve our understanding of gemcitabine-resistance in pancreatic cancer.
机译：胰腺癌由于其快速发展，转移和对化学疗法的抵抗力，是影响消化系统的最恶性肿瘤之一。吉西他滨化疗通常是晚期胰腺癌的首选治疗方法。然而，化学抗性是成功治疗的主要障碍。为了阐明胰腺癌中吉西他滨耐药的潜在机制，使用人胰腺癌细胞系SW1990建立了耐药细胞株SW1990-吉西他滨（SW1990-GZ）。还使用3-（4,5-二甲基-2-噻唑基）-2,5-二苯基-2-H-溴化四氮唑（MTT）分析评估了SW1990和SW1990-GZ细胞的IC50，抗性指数和生长。使用高效液相色谱（HPLC）测量了SW1990和SW1990-GZ中吉西他滨的细胞吸收。还通过蛋白质印迹分析评估了p53的蛋白质表达。结果表明，SW1990-Gz的IC50分别为0.07±0.0021和87.5±3.24μg/ ml，SW1990-Gz的电阻指数比为1,250。与SW1990细胞相比，SW1990-GZ细胞的生长速率较低。 HPLC结果表明，与不同时间点的SW1990细胞相比，SW1990-GZ细胞的吉西他滨摄取明显减少。耐GEM的SW1990-GZ细胞的p53蛋白表达明显高于SW1990细胞（P <0.01）。这些结果表明，成功建立了具有稳定且显着的耐药性的人吉西他滨耐药的胰腺癌细胞系。本研究的结果表明，吉西他滨的细胞摄取减少可能在SW1990-GZ细胞的吉西他滨化学耐药中起重要作用。因此，该细胞系可以用作有效的体外模型，以增进我们对胰腺癌中吉西他滨耐药性的了解。

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