Celecoxib up-regulates the expression of the zeta chain of T cell receptor complex in tumor-infiltrating lymphocytes in human cervical cancer

Clin Cancer Res. 2006 Apr 1;12(7 Pt 1):2055-60. doi: 10.1158/1078-0432.CCR-05-2530.

Abstract

Purpose: We evaluated the effects of celecoxib treatment on tumor-infiltrating lymphocyte (TIL) subsets [CD3(+), CD4(+),CD8(+), CD25(+), and T cell receptor (TCR)-zeta-expressing cells] and tryptase-positive mast cells in cervical tumors. Circulating levels of cytokines [interleukin (IL)-1beta, IL-10, tumor necrosis factor-alpha, IL-6, and IL-12] and angiogenesis-modulating factors (vascular endothelial growth factor and endostatin) have also been analyzed.

Experimental design: Cervical tumor biopsies and blood samples were obtained at the time of diagnosis and after 10 days of celecoxib treatment (400 mg b.i.d., at 8:00 a.m. and 8:00 p.m.) in 27 cases. Immunohistochemistry and ELISA assays were used to assess the expression of biological factors in tumor tissue and circulating levels of cytokines and angiogenic molecules.

Results: We showed a statistically significant increase in the percentage of TIL expressing the TCR-zeta chain after celecoxib treatment: indeed, in cases exposed to celecoxib, the percentage of TCR-zeta(+) cells ranged from 5.0 to 50.0 (median, 22.5) with respect to baseline expression (range, 3.0-50.0; median, 10.0; P = 0.0016). There was no significant treatment-related difference in the percentage of CD3(+), CD4(+), CD8(+), and CD25(+) TIL as well as in tryptase-positive cells. IL-12 levels were significantly reduced in posttreatment samples with respect to baseline levels (P = 0.002). We also found a reduction in the circulating levels of vascular endothelial growth factor, and a statistically significant increase of serum endostatin levels (P = 0.035).

Conclusions: We reported the first evidence in humans that celecoxib restores zeta expression by TIL in primary cervical tumors, suggesting that a positive modulation of immune function may serve as an additional mechanism supporting the antitumor effect of this class of drugs.

Publication types

  • Clinical Trial
  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Celecoxib
  • Cytokines / drug effects
  • Cytokines / metabolism
  • Endostatins / drug effects
  • Endostatins / immunology
  • Enzyme-Linked Immunosorbent Assay
  • Female
  • Gene Expression Regulation / drug effects*
  • Gene Expression Regulation / genetics
  • Humans
  • Immunohistochemistry
  • Lymphocytes, Tumor-Infiltrating / drug effects*
  • Lymphocytes, Tumor-Infiltrating / immunology*
  • Membrane Proteins / genetics*
  • Membrane Proteins / metabolism*
  • Middle Aged
  • Patient Compliance
  • Pyrazoles / adverse effects
  • Pyrazoles / pharmacology*
  • Receptors, Antigen, T-Cell / genetics*
  • Receptors, Antigen, T-Cell / metabolism*
  • Sulfonamides / adverse effects
  • Sulfonamides / pharmacology*
  • Up-Regulation / drug effects
  • Up-Regulation / immunology
  • Uterine Cervical Neoplasms / diagnosis
  • Uterine Cervical Neoplasms / drug therapy
  • Uterine Cervical Neoplasms / immunology*
  • Vascular Endothelial Growth Factor A / drug effects
  • Vascular Endothelial Growth Factor A / immunology

Substances

  • Cytokines
  • Endostatins
  • Membrane Proteins
  • Pyrazoles
  • Receptors, Antigen, T-Cell
  • Sulfonamides
  • VEGFA protein, human
  • Vascular Endothelial Growth Factor A
  • antigen T cell receptor, zeta chain
  • Celecoxib