title: Expression of hPNAS-4 radiosensitizes Lewis lung cancer.
abstract: OBJECTIVE
  This study aimed to transfer the hPNAS-4 gene, a novel apoptosis-related human gene, into Lewis lung cancer (LL2) and observe its radiosensitive effect on radiation therapy in vitro and in vivo.
  
  
  METHODS
  The hPNAS-4 gene was transfected into LL2 cells, and its expression was detected via western blot. Colony formation assay and flow cytometry were used to detect the growth and apoptosis of cells treated with irradiation/PNAS-4 in vitro. The hPNAS-4 gene was transferred into LL2-bearing mice through tail vein injection of the liposome/gene complex. The tumor volumes were recorded after radiation therapy. Proliferating cell nuclear antigen (PCNA) immunohistochemistry staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay were performed to detect the tumor cell growth and apoptosis in vivo.
  
  
  RESULTS
  The hPNAS-4 gene was successfully transferred into LL2 cells and tumor tissue, and its overexpressions were confirmed via western blot analysis. Compared with the control, empty plasmid, hPNAS-4, radiation, and empty plasmid plus radiation groups, the hPNAS-4 plus radiation group more significantly inhibited growth and enhanced apoptosis of LL2 cells in vitro and in vivo (P<.05).
  
  
  CONCLUSIONS
  The hPNAS-4 gene was successfully transferred into LL2 cells and tumor tissue and was expressed in both LL2 cell and tumor tissue. The hPNAS-4 gene therapy significantly enhanced growth inhibition and apoptosis of LL2 tumor cells by radiation therapy in vitro and in vivo. Therefore, it may be a potential radiosensitive treatment of radiation therapy for lung cancer.
authors: Department of Radiation Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China.
authors: Hui
authors: H
authors: Zeng
authors: Zhu
authors: Z
authors: Yuan
authors: Hong
authors: H
authors: Zhu
authors: Lei
authors: L
authors: Li
authors: Huashan
authors: H
authors: Shi
authors: Zi
authors: Z
authors: Wang
authors: Yu
authors: Y
authors: Fan
authors: Qian
authors: Q
authors: Deng
authors: Jianshuang
authors: J
authors: Zeng
authors: Yinbo
authors: Y
authors: He
authors: Jianghong
authors: J
authors: Xiao
authors: Zhiping
authors: Z
authors: Li
mesh_terms: D000818:Animals; D017209:Apoptosis; D051017:Apoptosis Regulatory Proteins / Q000235:genetics / Q000378:metabolism*; D019759:Carbon-Nitrogen Lyases; D018827:Carcinoma, Lewis Lung / Q000378:metabolism* / Q000473:pathology / Q000628:therapy*; D045744:Cell Line, Tumor; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D020287:In Situ Nick-End Labeling / Q000379:methods; D008175:Lung Neoplasms / Q000378:metabolism* / Q000473:pathology / Q000628:therapy*; D051379:Mice; D008810:Mice, Inbred C57BL; D009363:Neoplasm Proteins / Q000235:genetics / Q000378:metabolism*; D034741:RNA, Small Interfering / Q000494:pharmacology; D011897:Random Allocation; D014162:Transfection / Q000379:methods; D047368:Tumor Burden; D014410:Tumor Stem Cell Assay
chemical_list: D051017:Apoptosis Regulatory Proteins; D009363:Neoplasm Proteins; D034741:RNA, Small Interfering; D019759:Carbon-Nitrogen Lyases; C000604991:DESI2 protein, human