Development of the new radiation therapy using tumor suppressor gene NPRL2 for esophageal cancer

在10个人食管癌细胞系中，辐射的IC50为1.58 ~ 9.28Gy。NPRL2蛋白在这些细胞系中均未表达，而Rad51蛋白在所有细胞系中均有强表达。NPRL2或Rad51的表达水平与放射敏感性无关。NPRL2载体对人食管癌细胞的肿瘤生长抑制率约为30%，NPRL2载体与放射治疗的IC20联合治疗可将其抑制率提高至60%左右。我们制备了一些Rad51- sirna载体，但这些Rad51- sirna载体没有抑制Rad51蛋白的表达。为了探讨NPRL2载体联合作用的机制，我们将其分为四组；1)对照组，2)放射治疗（IC20）， 3) NPRL2组，4)NPRL2+放疗。与其他组相比，NPRL2+放疗组激活了DNA损伤通路，表现出较强的G2阻滞和细胞凋亡。

In 10 human esophageal cancer cell lines, the IC50 of radiation ranged from IC50 1.58Gy to 9.28Gy. There were no expression of NPRL2 protein in these cell lines, on the other hand, Rad51 protein showed strong expression in all cell lines. The levels of NPRL2 or Rad51 expression did not correlate with radiosensitivity. Tumor growth inhibition rate of NPRL2 vector was about 30% for human esophageal cancer cells, and combination therapy of NPRL2 vector and IC20 of radiation therapy enhanced this inhibitory effect to around 60 percent. We prepared some Rad51-siRNA vectors, however, these Rad51-siRNA vector did not inhibit expression of Rad51 protein. To investigate the mechanism of combined effect of NPRL2 vector, we made four groups ; 1) control group, 2) radiation therapy (IC20), 3) NPRL2 group, 4) NPRL2+radiotherapy. NPRL2+radiation therapy groupactivated DNA damage pathway, and showed a strong G2 arrest and apoptosis, compared with the other group.