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首页> 外文期刊>Scandinavian journal of gastroenterology. >Expressions of urokinase-type plasminogen activator, its receptor and plasminogen activator inhibitor-1 in gastric cancer cells and effects of Helicobacter pylori.
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Expressions of urokinase-type plasminogen activator, its receptor and plasminogen activator inhibitor-1 in gastric cancer cells and effects of Helicobacter pylori.

机译：尿激酶型纤溶酶原激活物，其受体和纤溶酶原激活物抑制剂-1在胃癌细胞中的表达及幽门螺杆菌的作用。

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摘要

Destruction of the extracellular matrix is essential for tumor invasion and metastasis. The relationship between Helicobacter pylori (H. pylori) infection and destruction of the extracellular matrix is not yet clear. Urokinase-type plasminogen activator (uPA) plays an important role in the destruction of the extracellular matrix and basement membrane. Urokinase-type plasminogen activator receptor (uPAR) and plasminogen activator inhibitor-1(PAI-1) appear to be associated with these processes. To clarify the role of H. pylori infection in the processes of destruction of the extracellular matrix and basement membrane in cancerous tissue, the effect of H. pylori on the expressions of uPA, uPAR and PAI-1 in cancer cells was investigated.Gastric cancer cell lines (MKN45, KATO-III) were co-cultured with H. pylori standard strain (NCTC11637), cagA-negative strain and clinical isolated strain. The specific inductions of uPA, uPAR and PAI-1 mRNA were examined by reverse transcription-polymerase chain reaction (RT-PCR) amplification. The secreted uPA antigen was measured by enzyme-linked immunosorbent assay (ELISA). To evaluate the role of transcription factor NF-kappaB in uPA and uPAR gene transcription with H. pylori stimulation, the effect of NF-kappaB inhibitor MG132 on H. pylori-induced uPA and uPAR mRNA expression was examined.The expressions of both uPA and uPAR mRNAs in the gastric cancer cell lines (MKN45 and KATO- III) were increased markedly (uPA mRNA; MKN45: 12-fold, KATO-III: 5-fold) (uPAR mRNA; MKN45: 3-fold, KATO-III: 3-fold) with H. pylori NCTC11637 strain stimulation, whereas the expression levels of uPA and uPAR mRNA did not increase with cagA-negative strain stimulation. These cancer cell lines slightly secreted uPA antigen into the culture medium, and the amount of uPA antigen increased dramatically by stimulation with H. pylori NCTC11637 and cagA-positive clinical isolated strains. These gastric cancer cell lines also slightly secreted PAI-1 antigen into the culture medium, and the amount of PAI-1 antigen was not affected by H. pylori NCTC11637 stimulation. H. pylori-induced uPA and uPAR mRNA expressions were strongly down-regulated by pretreatment with MG132 in both cell lines.The results of this study indicated the possibility that cagA-positive H. pylori may play an important role not only in tissue remodeling, angiogenesis and wound healing but also in the process of degradation of the extracellular matrix breakdown, tumor invasion and metastasis by inducing uPA and uPAR complex in the gastric cancer cells.
机译：细胞外基质的破坏对于肿瘤的侵袭和转移至关重要。幽门螺杆菌（H. pylori）感染与细胞外基质破坏之间的关系尚不清楚。尿激酶型纤溶酶原激活剂（uPA）在破坏细胞外基质和基底膜中起重要作用。尿激酶型纤溶酶原激活物受体（uPAR）和纤溶酶原激活物抑制剂-1（PAI-1）似乎与这些过程有关。为了阐明幽门螺杆菌感染在癌组织细胞外基质和基底膜破坏过程中的作用，研究了幽门螺杆菌对癌细胞中uPA，uPA​​R和PAI-1表达的影响。将细胞系（MKN45，KATO-III）与幽门螺杆菌标准菌株（NCTC11637），cagA阴性菌株和临床分离菌株共培养。通过逆转录-聚合酶链反应（RT-PCR）扩增检查了uPA，uPA​​R和PAI-1 mRNA的特异性诱导。通过酶联免疫吸附测定（ELISA）测量分泌的uPA抗原。为了评估幽门螺杆菌刺激下转录因子NF-kappaB在uPA和uPAR基因转录中的作用，检测了NF-kappaB抑制剂MG132对幽门螺杆菌诱导的uPA和uPAR mRNA表达的影响.uPA和uPAR的表达胃癌细胞系（MKN45和KATO-III）中的uPAR mRNA显着增加（uPA mRNA; MKN45：12倍，KATO-III：5倍）（uPAR mRNA; MKN45：3倍，KATO-III：幽门螺杆菌NCTC11637菌株刺激的3倍），而cagA阴性菌株刺激的uPA和uPAR mRNA的表达水平没有增加。这些癌细胞系将uPA抗原稍微分泌到培养基中，并且通过幽门螺杆菌NCTC11637和cagA阳性临床分离株的刺激，uPA抗原的量急剧增加。这些胃癌细胞系也将PAI-1抗原稍微分泌到培养基中，并且PAI-1抗原的量不受幽门螺杆菌NCTC11637刺激的影响。 MG132预处理可在两种细胞系中强烈抑制幽门螺杆菌诱导的uPA和uPAR mRNA表达。这项研究结果表明，cagA阳性幽门螺杆菌不仅在组织重塑中可能起重要作用，通过在胃癌细胞中诱导uPA和uPAR复合物，血管生成和伤口愈合以及细胞外基质降解，肿瘤侵袭和转移的降解过程中。

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