TargetRx Atlas

MRNA basic information

  • mRNA ID:ENST00000367468
  • Gene Name:PTGS2
  • mRNA database:Ensembl
  • mRNA expression :down-regulated
  • mRNA Method:RT-PCR
  • mRNA Pathway:COX pathway
  • Evidence:validated
  • (mRNA-drug)

Drug basic information

  • Drug ID:NA
  • Drug Name:Gleditsia sinensis
  • Drug Method:down-regulated the gene expression the gene expression

Disease basic infommation

  • Disease:esophageal cancer
  • Tissue:cell lines (KYSE 30, KYSE 150, KYSE 450, KYSE 510, KYSE 520, HKESC-3, HKESC-4 ,SLMT-1)

Other information

  • Title:The inhibitory effect of Gleditsia sinensis on cyclooxygenase-2 expression in human esophageal squamous cell carcinoma
  • Journal:Int J Mol Med
  • Published:2009
  • PubMed ID:19082515
  • Abstract:The anti-cancer effects of the anomalous fruit extract of Gleditsia sinensis (GSE) attributed to its apoptotic activity, telomerase inhibition and anti-angiogenesis in a panel of solid and non-solid tumor cell lines including esophageal squamous cell carcinoma (ESCC) have been intensively investigated by us in previous studies. Cyclooxygenase-2 (COX-2) has been well described as another promising target of cancer therapy for ESCC, and novel therapeutic agents are still being sought which target COX-2 expression. However, the anti-cancer effect of GSE through the suppression of COX-2 expression has not been previously investigated. In the present study, the anti-cancer effects of GSE on eight ESCC cell lines (KYSE 30, KYSE 150, KYSE 450, KYSE 510, KYSE 520, HKESC-3, HKESC-4 and SLMT-1) of Chinese and Japanese origins were first studied by MTS cytotoxicity assays. The effects of GSE on COX-2 expression levels and on the housekeeping form COX-1 were also investigated by multiplex RT-PCR analysis. Moreover, the anti-proliferative effect of GSE on KYSE 510 was also studied by anchorage-independent clonogenicity assay in soft agar. The results showed that GSE induced a dose- and time-dependent cytotoxicity on all of the eight ESCC cell lines and caused positive anti-proliferative action on KYSE 510 in the anchorage-independent clonogenicity assay, suggesting that GSE suppressed the in vitro growth of the ESCC cell lines. More importantly, the MRNA expression levels of COX-2, but not COX-1, in all of the ESCC cell lines were suppressed by GSE in a dose-dependent fashion. The overall results of the present study show that the anti-cancer effect of GSE on the ESCC cell lines is associated with the suppression of COX-2 expression, but not COX-1. Our findings also open a new chapter for the future advancement of GSE as a novel anti-cancer agent or as an adjuvant of traditional cancer treatments.
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