Department of Radiation Oncology, Osaka University Graduate School of Medicine.
J Radiat Res. 2011;52(3):374-9. doi: 10.1269/jrr.10102. Epub 2011 Feb 19.
We previously showed that carbon ion irradiation can inhibit the expression of the anillin (ANLN) gene, which is regulated by the activation of the phosphatidylinositol-3-kinase (PI3K)/Akt signaling pathway associated with metastasis. The purpose of this study is to compare the effects of carbon ion irradiation on the PI3K/Akt signaling pathway to those of photon irradiation. Our study showed that carbon ion irradiation of human lung adenocarcinoma cells A549 decreased their invasion more effectively than photon irradiation did. We found that carbon ion irradiation reduced the nuclear localization of ANLN at lower dose, but did not affect its expression. Low-dose carbon ion irradiation also reduced the level of phosphorylated Akt compared to untreated controls, whereas photon irradiation did not. These results suggest that carbon ion irradiation effectively suppresses the metastatic potential of A549 cells by suppressing the PI3K/Akt signaling pathway.
我们之前曾表明,碳离子照射可以抑制与转移相关的磷酸肌醇-3-激酶(PI3K)/ Akt 信号通路的激活所调控的肌动蛋白(ANLN)基因的表达。本研究的目的是比较碳离子照射对 PI3K/Akt 信号通路的影响与光子照射的影响。我们的研究表明,碳离子照射人肺腺癌细胞 A549 可更有效地抑制其侵袭能力。我们发现,碳离子照射在较低剂量下减少了 ANLN 的核定位,但不影响其表达。与未经处理的对照组相比,低剂量碳离子照射还降低了磷酸化 Akt 的水平,而光子照射则没有。这些结果表明,碳离子照射通过抑制 PI3K/Akt 信号通路有效抑制了 A549 细胞的转移潜能。