Department of Gastroenterology, Gifu University Graduate School of Medicine, Gifu 501-1194, Japan.
Oncol Rep. 2012 Apr;27(4):935-9. doi: 10.3892/or.2011.1612. Epub 2011 Dec 23.
We have recently reported that short wavelength ultraviolet-C (UVC) irradiation inhibits cell growth and induces apoptosis in human pancreatic cancer cells. In this study, we investigated the effect of UVC on platelet-derived growth factor (PDGF)-BB-induced migration in pancreatic cancer cells, AsPC1 and BxPC3. In cell migration assays using a Boyden chamber Transwell, PDGF-BB exerted a maximum effect on migration of these cells at a dose of 70 ng/ml after 36 h of treatment. PDGF-BB also caused phosphorylation of p44/p42 mitogen-activated protein kinase (MAPK), stress-activated protein kinase/c-Jun-N-terminal kinase (SAPK/JNK) and Akt, but not of p38 MAPK in these cells. Pretreatment of these cells with UVC at a dose over 10 J markedly suppressed PDGF-BB-induced migration. Since UVC significantly inhibited PDGF-BB-induced phosphorylation of Akt, and subsequent glycogen synthase kinase (GSK) 3β, but not p44/p42 MAPK and SAPK/JNK, it is likely that UVC inhibits PDGF-BB-induced migration by suppressing the Akt-GSK3β pathway in pancreatic cancer cells. Taken together with our previous findings, UVC could be a useful tool for the treatment of patients with pancreatic cancer.
我们最近报道了短波紫外线-C（UVC）照射抑制人胰腺癌细胞生长并诱导其凋亡。在这项研究中，我们研究了 UVC 对血小板衍生生长因子（PDGF）-BB 诱导的胰腺癌细胞（AsPC1 和 BxPC3）迁移的影响。在使用 Boyden 室 Transwell 的细胞迁移测定中，PDGF-BB 在 36 小时的处理后以 70ng/ml 的剂量对这些细胞的迁移产生最大的影响。PDGF-BB 还导致这些细胞中 p44/p42 丝裂原活化蛋白激酶（MAPK）、应激激活蛋白激酶/c-Jun-N-末端激酶（SAPK/JNK）和 Akt 的磷酸化，但不导致 p38 MAPK 的磷酸化。这些细胞用超过 10J 的剂量的 UVC 预处理明显抑制了 PDGF-BB 诱导的迁移。由于 UVC 显著抑制了 Akt 和随后的糖原合酶激酶（GSK）3β的磷酸化，但不抑制 p44/p42 MAPK 和 SAPK/JNK，因此 UVC 可能通过抑制 Akt-GSK3β 途径抑制 PDGF-BB 诱导的胰腺癌细胞迁移。综合我们以前的研究结果，UVC 可能是治疗胰腺癌患者的有用工具。
