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首页> 外文期刊>Current therapeutic research, clinical and experimental. >Effects of a Histone Deacetylase Inhibitor, Sodium Butyrate, on 53-kDa Protein Expression and Sensitivity to Anticancer Drugs of Pancreatic Cancer Cells
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Effects of a Histone Deacetylase Inhibitor, Sodium Butyrate, on 53-kDa Protein Expression and Sensitivity to Anticancer Drugs of Pancreatic Cancer Cells

机译：组蛋白脱乙酰基酶抑制剂丁酸钠对胰腺癌细胞53 kDa蛋白表达和抗癌药物敏感性的影响

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BACKGROUND: Several tumor-suppressor genes, such as 53-kDa protein (p53), are inactivated in some pancreatic cancers. The lack of a functional p53 has been proposed to be a component of resistance to chemotherapy, resulting in the inhibition of apoptosis. Therefore, reintroduction of wild-type p53 is a commonly used gene therapy strategy for the treatment of various types of cancer, including pancreatic cancer.OBJECTIVE: The aim of this study was to examine the ability of the histone deacetylase inhibitor, sodium butyrate (NaB), to modulate the expression of p53.METHODS: Five human pancreatic carcinoma cell lines (SW-1990, BxPC-3, PANC-1, MIA PaCa-2, JHP-1) were utilized. Two of the cell lines (SW-1990 and JHP-1) lacked p53 expression, as determined by Western blot analysis, and were investigated further. Expression of p53 was determined by densitometry of all bands present in the Western blot. Drug sensitivity was measured with a tetrazolium-based assay by exposing the cells to graded concentrations of NaB and/or anticancer drugs (cisplatin, fluorouracil, SN-38, and paclitaxel). Apoptosis was observed using gel electrophoresis.RESULTS: In the SW-1990 and JHP-1 cell lines, use of 1 mM NaB was found to induce histone acetylation and p53 expression compared with those not treated with NaB (P = 0.01 and P = 0.018, respectively). Sensitivity to cisplatin (P = 0.021), fluorouracil (P = 0.046), and SN-38 (P = 0.039) was significantly enhanced by NaB treatment compared with nontreatment. However, sensitivity to paclitaxel was not significantly different between untreated and NaB-treated cells. A higher frequency of apoptosis was observed in NaB-treated cells compared with that of control cells.Conclusion: This in vitro study found that NaB induced p53 expression in 2 pancreatic cancer cell lines (SW-1990 and JHP-1). Moreover, NaB acted on a biochemical modulator for antieuplastic therapy. Future research is necessary to assess the value of these findings.
机译：背景：在某些胰腺癌中，一些肿瘤抑制基因（例如53 kDa蛋白（p53））被灭活。已提出缺乏功能性p53是对化学疗法具有抗性的成分，从而导致凋亡的抑制。因此，重新引入野生型p53是治疗各种类型癌症（包括胰腺癌）的常用基因治疗策略。目的：这项研究的目的是检验组蛋白脱乙酰基酶抑制剂丁酸钠（NaB）的能力。方法：调节五种人胰腺癌细胞系（SW-1990，BxPC-3，PANC-1，MIA PaCa-2，JHP-1）。通过蛋白质印迹分析确定其中两个细胞系（SW-1990和JHP-1）缺乏p53表达，并进行了进一步研究。通过在蛋白质印迹中存在的所有条带的光密度测定法确定p53的表达。通过将细胞暴露于分级浓度的NaB和/或抗癌药（顺铂，氟尿嘧啶，SN-38和紫杉醇）中，通过基于四唑鎓的测定法来测量药物敏感性。结果：在凝胶电泳中观察到了细胞凋亡。结果：在SW-1990和JHP-1细胞系中，与未用NaB处理的细胞相比，使用1 mM NaB可以诱导组蛋白乙酰化和p53表达（P = 0.01和P = 0.018）。 ， 分别）。与未治疗相比，NaB治疗显着提高了对顺铂（P = 0.021），氟尿嘧啶（P = 0.046）和SN-38（P = 0.039）的敏感性。但是，未经处理和经NaB处理的细胞对紫杉醇的敏感性无明显差异。结论：该体外研究发现，NaB诱导了2种胰腺癌细胞系（SW-1990和JHP-1）中p53的表达。此外，NaB在抗肿瘤治疗的生化调节剂上起作用。未来的研究对于评估这些发现的价值是必要的。

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