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胰腺癌是一种常见的消化系统肿瘤,其恶性程度和致死率高。临床上用于治疗胰腺癌的化疗药物如吉西他滨,具有较高的毒副作用,因此开发低毒性的新型抗癌药物具有重要意义。文章对金环蛇Cathelicidin基因编码的多肽BF-30对鼠源胰腺癌细胞Panc02的体外抗肿瘤活性进行了研究。CCK-8检测结果表明,BF-30体外可以抑制Panc02细胞的增殖,IC50为(21.6±0.8)μmol/L,且呈时间和剂量依赖关系。透射电子显微镜(TEM)结果显示,BF-30对Panc02细胞膜具有穿透作用。当细胞膜失去完整性时,乳酸脱氢酶(LDH)可释放到细胞外,PI染色阳性率升高。同时,BF-30可以与基因组DNA结合,剂量依赖性抑制VEGF mRNA表达,并抑制Panc02细胞迁移。因此,BF-30可通过穿透细胞膜,结合基因组DNA,抑制细胞迁移,进而抑制Panc02细胞的增殖。BF-30作为抗胰腺癌药物具有良好的应用前景。
Pancreatic cancer is a common digestive system tumor with a high degree of malignancy and lethality. Clinically used to treat pancreatic cancer chemotherapy drugs such as gemcitabine, has a higher toxicity, therefore, the development of low toxicity of new anti-cancer drugs of great significance. The antitumor activity of murine pancreatic cancer cell Panc02 was studied in vitro by using the polypeptide BF-30 encoded by the Cathelicidin gene. The results of CCK-8 assay showed that BF-30 could inhibit the proliferation of Panc02 cells in vitro with IC50 of (21.6 ± 0.8) μmol / L in a time-and dose-dependent manner. Transmission electron microscopy (TEM) results showed that BF-30 had a penetrating effect on Panc02 cell membrane. When the integrity of the cell membrane is lost, lactate dehydrogenase (LDH) is released to the outside of the cell and the positive rate of PI staining is increased. Meanwhile, BF-30 can bind to genomic DNA, inhibit VEGF mRNA expression in a dose-dependent manner, and inhibit the migration of Panc02 cells. Therefore, BF-30 can inhibit the proliferation of Panc02 cells by penetrating the cell membrane, binding genomic DNA and inhibiting cell migration. BF-30 as a pancreatic cancer drug has a good prospect.