Asan Digestive Disease Research Institute and Asan Institute for Life Sciences, Seoul, Korea.
Cancer Invest. 2011 May;29(4):257-65. doi: 10.3109/07357907.2011.568562.
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.
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。