摘要
目的:探讨Ras p21蛋白活化子1(Ras p21 protein activator 1,RASA1)在胰腺癌中的表达状况及可能作用。方法:以qRT-PCR检测胰腺癌细胞(Capan-2、CFPAC-1、BxPC-3)和胰腺导管上皮细胞(H6C7)中RASA1 mRNA表达水平的差异,以Western blotting检测上述细胞之间RASA1蛋白表达水平的差异;以免疫组化检测RASA1蛋白在胰腺癌及胰腺良性病变(慢性胰腺炎、胰腺囊肿)中的表达差异,并观察其表达水平与胰腺癌各临床病理因素之间的联系。结果:各胰腺癌细胞株中RASA1 mRNA和蛋白表达水平均低于胰腺导管上皮细胞(P<0.05)。肿瘤组织RASA1蛋白表达水平显著低于良性病变组织(P<0.05);侵犯周边器官的肿瘤组织中RASA1表达显著低于局限于胰腺内的组织(P<0.05);Ⅰ期胰腺癌组织RASA1的表达则显著高于Ⅱ、Ⅲ期的癌组织(P<0.05);但RASA1表达与胰腺癌的远处转移关系尚不明确。结论:RASA1作为抑癌蛋白可能在胰腺癌的发生发展中发挥重要作用。
AIM: To investigate the role of Ras p21 protein activator 1 (RASA1) in the development and progress of pancreatic cancer. METHODS: Different expression levels of RASA1 were measured by qRT-PCR and Western blotting in the pancreatic cancer cells Capan-2, CFPAC-1 and BxPC-3, and the pancreatic ductal cell line H6C7. Besides, the different expression levels between the pancreatic cancer and the pancreatic benign lesions, such as chronic pancreatitis or pancreatic cyst, were detected by the method of immunohistochemistry. The relationship between the clinicopathological feature and the RASA1 expression was analyzed. RESULTS: Both mRNA and protein expression levels of RASA1 decreased in pancreatic cancer cells compared with the ones in the pancreatic ductal cells (P〈0.05). The protein level of RASA1 in the pancreatic cancer tissues was lower than that in the pancreatic benign lesion tissues (P〈0.05). The pancreatic cancer samples with adjacent organ invasion had a significantly lower expression level of RASA1 than that in the pancreatic cancer samples limited in the pancreas (P〈0.05). The expression levels of RASA1 were much higher in the cancers on stage I than the ones on stage II or Ⅲ (P〈0.05). However, no relationship between the RASA1 expression level and the maximum diameter of cancer, the lymph node invasion and the survival time was observed. CONCLUSION: RASA1 plays an important role in the pancreatic cancer development as a potential tumor suppressor.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2012年第6期991-995,共5页
Chinese Journal of Pathophysiology
基金
广东省科技计划(No.2010B050700014
No.2011B0318000004)