目的:探讨microRNA-10b(miR-10b)与胰腺癌细胞吉西他滨(gemcitabine,GEM)化疗耐药的相关性及可能机制。方法:RT-qPCR检测吉西他滨相对耐药的胰腺癌细胞株PANC-1及吉西他滨相对敏感的CFPAC-1中miR-10b的表达情况;用不同浓度的吉西他滨作用于上述细胞,RT-qPCR检测二者miR-10b的表达变化;CFPAC-1细胞转染miR-10b mimics上调miR-10b表达量,CCK-8法及流式细胞仪检测细胞对吉西他滨药物敏感性的变化,Western blot检测抗凋亡相关蛋白(如PI3K、p-Akt、Bcl-2、Survivin)的表达,RT-qPCR检测PTEN基因的表达变化。结果:PANC-1细胞中miR-10b的表达显著高于CFPAC-1细胞,且上述两种细胞中miR-10b的表达量与吉西他滨呈浓度梯度依赖;高表达miR-10b后CFPAC-1细胞对吉西他滨的敏感性下降,PI3K、p-Akt、Bcl-2、Survivin蛋白的表达升高,PTEN mRNA的表达水平降低。结论:miR-10b可能通过负性调控PTEN的表达水平,从而增加PI3K、p-Akt、Bcl-2、Survivin蛋白的表达,减少凋亡来降低CFPAC-1对吉西他滨的敏感性,最终导致胰腺癌细胞对吉西他滨化疗耐受。 OBJECTIVE: To investigate the correlation and possible mechanism of microRNA-10b (miR-10b) and chemosensitivity to gemcitabine (GEM) in pancreatic cancer cells. Methods: The expression of miR-10b in gemcitabine-resistant pancreatic cancer cell line PANC-1 and gemcitabine-sensitive CFPAC-1 was detected by RT-qPCR. The cells were treated with different concentrations of gemcitabine and detected by RT-qPCR miR-10b mimics up-regulated the expression of miR-10b in CFPAC-1 cells, the sensitivity of cells to gemcitabine was detected by CCK-8 assay and flow cytometry, and the anti-apoptosis was detected by Western blot (Such as PI3K, p-Akt, Bcl-2, Survivin) expression, RT-qPCR detection of PTEN gene expression changes. Results: The expression of miR-10b in PANC-1 cells was significantly higher than that in CFPAC-1 cells, and the expression levels of miR-10b in these two cells were concentration-dependently dependent on the concentration of gemcitabine. The sensitivity of gemcitabine decreased, the expression of PI3K, p-Akt, Bcl-2, Survivin protein increased and the expression level of PTEN mRNA decreased. Conclusions: miR-10b may decrease the sensitivity of CFPAC-1 to gemcitabine and may eventually lead to pancreatic cancer by negatively regulating the expression of PTEN, thereby increasing the expression of PI3K, p-Akt, Bcl-2 and Survivin proteins and decreasing apoptosis Cells are resistant to gemcitabine chemotherapy.