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New Therapeutic Schedule for Prostatic Cancer-3 Cells with ET-1 RNAi and Endostar

  • Zhang, Hao-Jie (Department of Urology Surgery, Huadong Hospital Affiliated To Fudan University) ;
  • Qian, Wei-Qing (Department of Urology Surgery, Huadong Hospital Affiliated To Fudan University) ;
  • Chen, Ran (Department of Urology Surgery, Huadong Hospital Affiliated To Fudan University) ;
  • Sun, Zhong-Quan (Department of Urology Surgery, Huadong Hospital Affiliated To Fudan University) ;
  • Song, Jian-Da (Department of Urology Surgery, Huadong Hospital Affiliated To Fudan University) ;
  • Sheng, Lu (Department of Urology Surgery, Huadong Hospital Affiliated To Fudan University)
  • Published : 2015.01.06

Abstract

Background: Endothelin-1 and Endostar are both significant for the progression, proliferation, metastasis and invasion of cancer. In this paper, we studied the effect of ET-1 RNAi and Endostar in PC-3 prostatic cancer cells. Materials and Methods: The lentiviral vector was used in the establishment of ET-1 knockdown PC-3 cells. Progression and apoptosis were assessed by CKK-8 and flow cytometry, respectively. Transwell assay was used to estimate invasion and signaling pathways were studied by Western blotting. Results: ET-1 mRNA and protein in ET-1 knockdown PC-3 cells were reduced to 26.4% and 22.4% compared with control group, respectively. ET-1 RNAi and Endostar both were effective for the suppression of progression and invasion of PC-3 cells. From Western blotting results, the effects of ET-1 regulation and Endostar on PC-3 cells were at least related to some signaling pathways involving PI3K/Akt/Caspase-3, Erk1/2/Bcl-2/Caspase-3 and MMPs (MMP-2 and MMP-9). Furthermore, combined treatment of ET-1RNAi and Endostar was found to be more effective than single treatment. Conclusions: Both ET-1 RNAi and Endostar can inhibit the progression and invasion of PC-3 cells, but combined treatment might be a better therapeutic schedule.

Keywords

ET-1 RNAi;endostar;PC-3 cells;apoptosis;proliferation;invasion

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