High expression of cyclooxygenase-2 in uterine fibroids and its correlation with cell proliferation

Eur J Obstet Gynecol Reprod Biol. 2013 Jun;168(2):199-203. doi: 10.1016/j.ejogrb.2013.01.006. Epub 2013 Feb 9.

Abstract

Objective: To investigate the expression of cyclooxygenase-2 (COX-2) in uterine fibroids and healthy uterine smooth muscle as well as its role in the pathogenesis of uterine fibroids.

Methods: We collected uterine fibroid tissues and their paired adjacent healthy uterine smooth muscle tissues from 30 cases of uterine fibroids. We used immunohistochemistry and quantitative real-time PCR, as well as western blot to detect COX-2 expression. Using the COX-2 inhibitors NS-398 and celecoxib, we observed the response to the inhibitors in the healthy and fibroid smooth muscle cell pairs.

Results: COX-2 was detected by immunohistochemistry in both uterine fibroids and uterine smooth muscle, with higher immunoreactivity in uterine fibroids; the positive index of the smooth muscle cells was 11.90 and the positive index of uterine fibroids cells was 46.50 (P<0.05). The expression of COX-2 mRNA in uterine fibroids was higher (0.122±0.062) than in normal smooth muscle tissue (0.025±0.009; P<0.05). Also, the western blot results showed that COX-2 expression was significantly higher in uterine fibroid cases, as compared to the expression in uterine smooth muscle. Immunofluorescence showed that the occurrence of COX-2 was obviously higher in smooth muscle cells of uterine fibroids than in the healthy smooth muscle cells. NS-398 or celecoxib significantly inhibited the proliferation of smooth muscle cells of uterine fibroids, but did not inhibit the proliferation of healthy smooth muscle cells. Accordingly, NS-398 or celecoxib significantly reduced the expression of the downstream metabolite of COX-2, PGE2, in the smooth muscle cells of uterine fibroids, but not in healthy smooth muscle cells.

Conclusion: COX-2 expression in uterine fibroids was significantly higher than in healthy uterine smooth muscles. The inhibition of COX-2 activity significantly reduced the proliferation of smooth muscle cells of the uterine fibroids, suggesting that COX-2 plays an important role in the pathogenesis of uterine fibroids.

MeSH terms

  • Adult
  • Antineoplastic Agents / pharmacology
  • Blotting, Western
  • Cell Proliferation / drug effects
  • Cells, Cultured
  • Cyclooxygenase 2 / chemistry
  • Cyclooxygenase 2 / genetics
  • Cyclooxygenase 2 / metabolism*
  • Cyclooxygenase 2 Inhibitors / pharmacology
  • Dinoprostone / antagonists & inhibitors
  • Dinoprostone / metabolism
  • Enzyme Induction*
  • Female
  • Humans
  • Immunohistochemistry
  • Leiomyoma / drug therapy
  • Leiomyoma / metabolism*
  • Leiomyoma / pathology
  • Leiomyoma / surgery
  • Middle Aged
  • Myometrium / drug effects
  • Myometrium / metabolism*
  • Myometrium / pathology
  • Myometrium / surgery
  • Neoplasm Proteins / antagonists & inhibitors
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / metabolism*
  • RNA, Messenger / metabolism
  • Real-Time Polymerase Chain Reaction
  • Tumor Cells, Cultured
  • Uterine Neoplasms / drug therapy
  • Uterine Neoplasms / metabolism*
  • Uterine Neoplasms / pathology
  • Uterine Neoplasms / surgery

Substances

  • Antineoplastic Agents
  • Cyclooxygenase 2 Inhibitors
  • Neoplasm Proteins
  • RNA, Messenger
  • Cyclooxygenase 2
  • PTGS2 protein, human
  • Dinoprostone