title: Antitumor activity of the selective cyclooxygenase-2 inhibitor, celecoxib, on breast cancer in Vitro and in Vivo.
abstract: BACKGROUND
  Cyclooxygenase-2(COX-2) promotes carcinogenesis, tumor proliferation, angiogenesis, prevention of apoptosis, and immunosuppression. Meanwhile, COX-2 over-expression has been associated with tumor behavior and prognosis in several cancers. This study investigated the antitumor effects of the selective COX-2 inhibitor, Celecoxib, on breast cancer in vitro and in vivo.
  
  
  METHODS
  Human breast cancer MCF-7 and MDA-MB-231 cells were cultured with different concentration (10, 20, 40 μmol/L) of celecoxib after 0-96 hours in vitro. MTT assay was used to determine the growth inhibition of breast cancer cells in vitro. The expression of COX-2 on mRNA was measured by real-time quantitive PCR analysis. Flow cytometry was performed to analyze the cell cycle of MCF-7 cells. Levels of PGE2 were measured by ELISA method. The in vivo therapeutic effects of celecoxib were determined using rat breast cancer chemically induced by 7,12-dimethylben anthracene (DMBA).
  
  
  RESULTS
  The inhibition of proliferation of both MCF-7 and MDA-MB-231 cells in vitro by celecoxib was observerd in time and dose dependent manner. Celecoxib effectively down-regulated the expression of COX-2. The cell cycle was arrested at G0/G1, and rate of cells in S phase was obviously decreased. Levels of PGE2 were inhibited by Celecoxib. The tumor incidence rate of the celecoxib group was lower than that of the control group. In addition, the tumor latency period of the celecoxib group was longer than that of the control group.
  
  
  CONCLUSIONS
  Celecoxib inhibited the proliferation of breast cancer cell lines in vitro, and prevented the occurrence of rat breast cancer chemically induced by DMBA. Therefore, celecoxib exhibits an antitumor activity and seems to be effective in anti-tumor therapy.
authors.affiliation: Department of Oncology, the Second Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, 710004, China.
authors.forename: Zhi-Jun
authors.initials: ZJ
authors.lastname: Dai
authors.affiliation: Department of Oncology, the Second Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, 710004, China.
authors.forename: Xiao-Bin
authors.initials: XB
authors.lastname: Ma
authors.affiliation: Department of Oncology, the Second Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, 710004, China.
authors.forename: Hua-Feng
authors.initials: HF
authors.lastname: Kang
authors.affiliation: Department of Oncology, the Second Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, 710004, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Gao
authors.affiliation: Department of Oncology, the Second Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, 710004, China.
authors.forename: Wei-Li
authors.initials: WL
authors.lastname: Min
authors.affiliation: Department of Oncology, the Second Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, 710004, China.
authors.forename: Hai-Tao
authors.initials: HT
authors.lastname: Guan
authors.affiliation: Department of Oncology, the Second Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, 710004, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Diao
authors.affiliation: Department of Oncology, the Second Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, 710004, China.
authors.forename: Wang-Feng
authors.initials: WF
authors.lastname: Lu
authors.affiliation: Department of Oncology, the Second Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, 710004, China.
authors.forename: Xi-Jing
authors.initials: XJ
authors.lastname: Wang