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15-羟基前列腺素脱氢酶在胃癌中下调并表现出肿瘤抑制活性。

15-hydroxyprostaglandin dehydrogenase is downregulated and exhibits tumor suppressor activity in gastric cancer.

机构信息

Asan Digestive Disease Research Institute and Asan Institute for Life Sciences, Seoul, Korea.

出版信息

Cancer Invest. 2011 May;29(4):257-65. doi: 10.3109/07357907.2011.568562.

Abstract

We investigated the tumor suppressor activity and regulatory mechanism of 15-hydroxyprostaglandin dehydrogenase (15-PGDH) in gastric cancer; 15-PGDH expression was lost in 70.1% of malignant human gastric tissues, but was preserved in normal and metaplastic gastritis. KATO III and SNU-719 cells were transfected with pcDNA3.1-empty vector or an expression vector encoding wild-type 15-PGDH. In TUNEL assays apoptotic cell numbers were increased in KATO-PGDH-WT cells compared with control. We found that EGFR and ERK1/2 inhibitors clearly increased the expression of 15-PGDH in KATO III cells. Our findings demonstrate both downregulation and a tumor suppressor activity of 15-PGDH in gastric cancer.

摘要

我们研究了 15-羟基前列腺素脱氢酶(15-PGDH)在胃癌中的肿瘤抑制活性和调节机制;在 70.1%的恶性人类胃组织中丢失了 15-PGDH 的表达,但在正常和化生性胃炎中保留了 15-PGDH 的表达。KATO III 和 SNU-719 细胞用 pcDNA3.1-空载体或编码野生型 15-PGDH 的表达载体转染。在 TUNEL 测定中,与对照相比,KATO-PGDH-WT 细胞中的凋亡细胞数量增加。我们发现,EGFR 和 ERK1/2 抑制剂可明显增加 KATO III 细胞中 15-PGDH 的表达。我们的研究结果表明,15-PGDH 在胃癌中既下调又具有肿瘤抑制活性。

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