title: New therapeutic schedule for prostatic cancer-3 cells with ET-1 RNAi and Endostar.
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.
  
  
  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.
authors.affiliation: Department of Urology Surgery, Huadong Hospital Affiliated To Fudan University, Shanghai, China E-mail : ditiandi1@163.com.
authors.forename: Hao-Jie
authors.initials: HJ
authors.lastname: Zhang
authors.forename: Wei-Qing
authors.initials: WQ
authors.lastname: Qian
authors.forename: Ran
authors.initials: R
authors.lastname: Chen
authors.forename: Zhong-Quan
authors.initials: ZQ
authors.lastname: Sun
authors.forename: Jian-Da
authors.initials: JD
authors.lastname: Song
authors.forename: Lu
authors.initials: L
authors.lastname: Sheng
mesh_terms: D017209:Apoptosis / Q000187:drug effects / Q000235:genetics*; D053148:Caspase 3 / Q000187:drug effects / Q000378:metabolism; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects / Q000235:genetics*; D043169:Endostatins / Q000494:pharmacology*; D019332:Endothelin-1 / Q000235:genetics*; D005786:Gene Expression Regulation / Q000187:drug effects / Q000235:genetics*; D055785:Gene Knockdown Techniques; D006801:Humans; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000187:drug effects / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000187:drug effects / Q000378:metabolism; D009361:Neoplasm Invasiveness; D019869:Phosphatidylinositol 3-Kinases / Q000187:drug effects / Q000378:metabolism; D011471:Prostatic Neoplasms / Q000235:genetics* / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000187:drug effects / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism*; D034741:RNA, Small Interfering / Q000494:pharmacology*; D011994:Recombinant Proteins; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D043169:Endostatins; D019332:Endothelin-1; D012333:RNA, Messenger; D034741:RNA, Small Interfering; D011994:Recombinant Proteins; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; C505407:CASP3 protein, human; D053148:Caspase 3; C522361:MMP2 protein, human; D020778:Matrix Metalloproteinase 2; C579270:MMP9 protein, human; D020780:Matrix Metalloproteinase 9; C522911:endostar protein