Increased expression of COX-2 in the development of human lung cancers

Takashi Takahashi, Ken Ichi Kozaki, Yasushi Yatabe, Hiroyuki Achiwa, Toyoaki Hida

Research output: Contribution to journalArticlepeer-review

37 Citations (Scopus)


It is well accepted that an increase in the expression of cyclooxygenase-2 (COX-2), a key inducible enzyme involved in the production of prostaglandins and other eicosanoids, may play a significant role in carcinogenesis in addition to its well-known role in inflammatory reactions. Whereas previous studies were largely confined to colorectal tumorigenesis, we have shown that a significantly increased expression of COX-2 may also play a role in the development of lung cancer. COX-2 expression was found to be frequently elevated in lung cancer, especially in adenocarcinoma, and the proportion of lung cancer cells with marked COX-2 expression was much higher in lymph node metastases than in the corresponding primary tumors. It was also shown that early stage adenocarcinoma patients with increased COX-2 expression who were surgically treated had a shorter survival. Our studies, which used high- and low-metastatic human lung cancer cell sublines established in our laboratory, revealed an association between metastatic capabilities and COX-2 expression levels: COX-2-specific inhibitors could inhibit in vitro the invasion of the highly metastatic NCI-H460-LNM35 clone through Matrigel-containing basement membrane components as well as the spontaneous in vivo metastasis in SCID mice. Taken together, these findings suggest that an increase in COX-2 expression may be associated with the development of lung cancer and possibly with the acquisition of an invasive and metastatic phenotype.

Original languageEnglish
Pages (from-to)177-181
Number of pages5
JournalJournal of Environmental Pathology, Toxicology and Oncology
Issue number2
Publication statusPublished - Jun 29 2002


  • COX-2
  • Carcinogenesis
  • Lung cancer
  • Metastasis

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Toxicology
  • Health, Toxicology and Mutagenesis


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