[Cyclooxygenase-2 expression in esophageal cancer cells and induction by mitomycin C]

Zhonghua Nei Ke Za Zhi. 2003 Oct;42(10):701-4.
[Article in Chinese]

Abstract

Objective: To study the relationship between COX-2 expression in esophageal cancer cell (EC/CUHK-1) and mitomycin C (MMC) treatment.

Methods: 2 mg/L of MMC was added to the well-grown EC/CUHK-1 cells cultured in RPMI-1640 including 10% FCS, and the medium was totally changed after 0.5, 1, 2, 4 and 8 h treatment, respectively. Cells were collected after another 24 h culture. Protein expression of COX-2, Bcl-2, Rb, p53 were examined by Western blot, and RT-PCR method was used to confirm the COX-2 expression in mRNA level. Cell cycle analysis for cells collected at 0, 0.5, 2, 4 and 8 h was performed on an EPICS profile analyzer.

Results: The cell cycle analysis showed that the percentage of apoptosis cells were (4.12 +/- 0.83)%, (1.00 +/- 0.11)%, (4.32 +/- 0.99)%, (9.46 +/- 2.11)% and (31.10 +/- 3.57)%, respectively. COX-2 mRNA expression were 2.60, 1.70, and 0.08 times, COX-2 protein expression were 2.0, 3.1 and 2.8 times, Bcl-2 protein were 3.6, 14.0 and 12.0 times, p53 protein were 1.8, 0.5 and 0.2 times, hyperphosphorylated form Rb were 8.2, 8.4 and 6.2 times, underphosphorylated form Rb were 1.8, 0.5 and 0.2 times in 0.5, 2 and 4 h after MMC treatment, respectively, as compared with the control group.

Conclusions: The COX-2 expression showed coincidence up-regulation according to the MMC-induced anti-apoptosis function activation in esophageal cancer cells, and the process was at least partly associated with Rb phosphorylation and p53 accumulation. It is implied that COX-2 may be a protecting factor in MMC induced esophageal cancer cell apoptosis, and the use of COX-2 inhibitor as an enhancer for esophageal cancer chemotherapy may be reasonable.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antibiotics, Antineoplastic / pharmacology*
  • Apoptosis*
  • Cyclooxygenase 2
  • Esophageal Neoplasms / enzymology
  • Esophageal Neoplasms / pathology
  • Gene Expression Regulation, Enzymologic / drug effects*
  • Humans
  • Isoenzymes / genetics
  • Isoenzymes / metabolism*
  • Membrane Proteins
  • Mitomycin / pharmacology*
  • Prostaglandin-Endoperoxide Synthases / genetics
  • Prostaglandin-Endoperoxide Synthases / metabolism*
  • RNA, Messenger / drug effects
  • RNA, Messenger / metabolism
  • Retinoblastoma Protein / metabolism
  • Tumor Cells, Cultured
  • Tumor Suppressor Protein p53 / metabolism
  • Up-Regulation / drug effects

Substances

  • Antibiotics, Antineoplastic
  • Isoenzymes
  • Membrane Proteins
  • RNA, Messenger
  • Retinoblastoma Protein
  • Tumor Suppressor Protein p53
  • Mitomycin
  • Cyclooxygenase 2
  • PTGS2 protein, human
  • Prostaglandin-Endoperoxide Synthases