antitumor activity of the selective cyclooxygenase-2 inhibitor, celecoxib, on breast cancer in vitro and in vivo选择性抗肿瘤活性cyclooxygenase-2抑制剂塞来昔布,乳腺癌在体外和体内.pdfVIP
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antitumor activity of the selective cyclooxygenase-2 inhibitor, celecoxib, on breast cancer in vitro and in vivo选择性抗肿瘤活性cyclooxygenase-2抑制剂塞来昔布,乳腺癌在体外和体内
Dai et al. Cancer Cell International 2012, 12:53
/content/12/1/53
PRIMARY RESEARCH Open Access
Antitumor activity of the selective
cyclooxygenase-2 inhibitor, celecoxib, on breast
cancer in Vitro and in Vivo
*† † *
Zhi-Jun Dai , Xiao-Bin Ma , Hua-Feng Kang , Jie Gao, Wei-Li Min, Hai-Tao Guan, Yan Diao, Wang-Feng Lu
*
and Xi-Jing Wang
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,
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