论文部分内容阅读
目的:观察胰腺组织及其癌变标本中基质金属蛋白酶(MatrixMetaloproteinases,MMPs)和金属蛋白酶的组织抑制物(TisueInhibitorsofMetaloproteinases,TIMPs)基因表达的变化关系,以探讨MMPs及其TIMPs在肿瘤侵袭和转移过程中的作用。方法:用原位杂交(insituhybridization,ISH)方法,采用cDNA探针(MMP2,MMP9,TIMP1)对两株胰腺癌细胞(Patu8988,Patu8902)、15例胰腺癌手术切除标本和8例正常胰腺组织标本进行了分子杂交检测。结果:MMP2(72-kDaIV型胶原酶)、MMP9(92-kDaIV型胶原酶)和TIMP1(0.9kb)的基因表达水平,在胰腺癌组织和间质细胞中,均有分布;MMP2在间质细胞中较多,TIMP1在胰腺癌组织和间质细胞中均匀分布,MMP9则多分布于肿瘤细胞中。结论:在胰腺癌组织中,MMP2、MMP9、TIMP1,可能参与了间质成分较强的降解反应过程,从而使肿瘤更易侵袭和转移;肿瘤和间质细胞似乎都能产生MMPs,TIMPs。
OBJECTIVE: To investigate the relationship between the expression of Matrix Metalloproteinases (MMPs) and Tissue Inhibitors of Metalloproteinases (TIMPs) in pancreatic tissues and their cancerous lesions to investigate the role of MMPs and TIMPs in tumor invasion and metastasis. effect. METHODS: In situ hybridization (ISH) method was used. cDNA probes (MMP2, MMP9, TIMP1) were used on two pancreatic cancer cells (Patu8988, Patu8902), 15 surgical specimens of pancreatic cancer and 8 normal pancreatic tissue specimens. Molecular hybridization tests were performed. Results: The gene expression levels of MMP2 (72-kDa type IV collagenase), MMP9 (92-kDa type IV collagenase) and TIMP1 (0.9kb) were distributed in pancreatic cancer tissues and interstitial cells; There are more in the mass of cells, and TIMP1 is evenly distributed in pancreatic cancer tissues and stromal cells. MMP9 is mostly distributed in tumor cells. CONCLUSIONS: In pancreatic cancer tissues, MMP2, MMP9, and TIMP1 may be involved in the process of degradation of interstitial components, making the tumor easier to invade and metastasize; tumors and interstitial cells seem to produce MMPs and TIMPs.