目的观察Rac1在胰腺癌组织及不同来源胰腺癌细胞中的表达情况,并检测其对癌细胞增殖和侵袭能力的影响。方法应用免疫组化法检测Rac1在胰腺癌组织中表达,并将癌组织按T分期进行分组,观察Rac1表达与病理分期之间的关系。通过RT-PCR、Western blot检测胰腺癌细胞株Rac1表达情况。用Rac1中和抗体对培养癌细胞进行干预,未干预组作为对照,通过MTT、Transwell方法检测Rac1对细胞增殖及侵袭能力的影响。结果与正常胰腺组织(0.07±0.17)相比,随着肿瘤分期的增加,Rac1在T1(0.37±0.08),T2(0.47±0.07),T3期(0.53±0.09)胰腺癌组织标本中表达呈上升趋势(P〈0.01)。Rac1在5株细胞中均呈阳性表达,应用Rac1中和抗体对培养癌细胞干预24 h,48 h及72 h,癌细胞的增殖能力均出现明显下降,其累计光密度值分别为1.49±0.07,1.53±0.03,1.55±0.04,与未加抗体组相比,差异有统计学意义(P〈0.01)。而培养20 h细胞的侵袭能力也明显降低,穿膜细胞数明显减少,与未加抗体组相比,差异有统计学意义(P〈0.05)。结论 Rac1在胰腺癌组织中高表达,并与肿瘤的分期明显相关。Rac1在胰腺癌细胞株中呈现普遍表达,可增强癌细胞的增殖及侵袭能力。
Objective To explore the expression of Rac1 in pancreatic tissue and cancer cell line,and its effects on the biological behavior of cancer cells. Methods The clinical and pathological features of formalin-ixed pancreatic cancer specimens and normal pancreases were analyzed. The expression of Rac1 was examined by immunohistochemistry. The relationship between the expression of Rac1 and tumor stage was analyzed. The expression of Rac1 in pancreatic cancer cells was examined by RT-PCR and Western blot.MTT and Transwell assays were used to observe the effect of high Rac1 expression on cell proliferation and invasion ability of pancreatic cancer cells. Results Rac1 was expressed in pancreatic cancer tissues,and the integral optical density(IOD)was 0. 07 ± 0. 17,0. 37± 0. 08,0. 47 ± 0. 07,0. 53 ± 0. 09 in normal tissues,tissues at stages T1,T2,T3,respectively. Rac1 expression was positively correlated with tumor stage(P 0. 01). Rac1 was also expressed in pancreatic cancer cell lines and overexpressed in Panc1. When the effect of Rac1 was neutralized by neutralizing antibody of Rac1 for 24,48,72 h,the proliferation was gradually inhibited with IOD of 1. 49± 0. 07,1. 53 ± 0. 03,1. 55 ± 0. 04,respectively(P 0. 01). The migration / invasion ability was also inhibited by neutralizing antibody(P 0. 05). Conclusion Rac1 is highly expressed in pancreatic cancer tissues and correlated with tumor stage. The Rac1 is expressed in cancer cell lines,and may increase the proliferation and migration / invasion of cancer cells.