A potential role for immunotherapy in thyroid cancer by enhancing NY-ESO-1 cancer antigen expression

Thyroid. 2014 Aug;24(8):1241-50. doi: 10.1089/thy.2013.0680. Epub 2014 Jun 30.

Abstract

Background: NY-ESO-1 is one of the most immunogenic members of the cancer/testis antigen family and its levels can be increased after exposure to demethylating and deacetylating agents. This cytoplasmic antigen can serve as a potent target for cancer immunotherapy and yet has not been well studied in differentiated thyroid cancer cells.

Methods: We studied the baseline expression of NY-ESO-1 messenger RNA and protein before and after exposure to 5-aza-2'-deoxycytidine (DAC) (72 hours) in a panel of thyroid cancer cell lines using quantitative polymerase chain reaction and Western blot. HLA-A2+, NY-ESO-1+ thyroid cell lines were then co-cultured with peripheral blood lymphocytes transduced with NY-ESO-1 specific T-cell receptor (TCR) and assayed for interferon-gamma and Granzyme-B release in the medium. SCID mice injected orthotopically with BCPAP cells were treated with DAC to evaluate for NY-ESO-1 gene expression in vivo.

Results: None of the thyroid cancer cell lines showed baseline expression of NY-ESO-1. Three cell lines, BCPAP, TPC-1, and 8505c, showed an increase in NY-ESO-1 gene expression with DAC treatment and were found to be HLA-A2 positive. DAC-treated target BCPAP and TPC-1 tumor cells with up-regulated NY-ESO-1 levels were able to mount an appropriate interferon-gamma and Granzyme-B response upon co-culture with the NY-ESO-1-TCR-transduced peripheral blood lymphocytes. In vivo DAC treatment was able to increase NY-ESO-1 expression in an orthotopic mouse model with BCPAP cells.

Conclusion: Our data suggest that many differentiated thyroid cancer cells can be pressed to express immune antigens, which can then be utilized in TCR-based immunotherapeutic interventions.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Antigens, Neoplasm / genetics*
  • Antigens, Neoplasm / metabolism*
  • Azacitidine / analogs & derivatives
  • Azacitidine / pharmacology
  • Cell Line, Tumor
  • Coculture Techniques
  • Cytoplasm / metabolism
  • Decitabine
  • Gene Expression Regulation
  • Gene Expression Regulation, Neoplastic*
  • Granzymes / metabolism
  • Humans
  • Immunotherapy / methods*
  • Interferon-gamma / metabolism
  • Lymphocytes / cytology
  • Membrane Proteins / genetics*
  • Membrane Proteins / metabolism*
  • Methylation
  • Mice
  • Mice, SCID
  • Neoplasm Metastasis
  • Polymerase Chain Reaction
  • RNA, Messenger / metabolism
  • Receptors, Antigen, T-Cell / metabolism
  • Thyroid Neoplasms / metabolism

Substances

  • Antigens, Neoplasm
  • CTAG1B protein, human
  • Membrane Proteins
  • RNA, Messenger
  • Receptors, Antigen, T-Cell
  • Decitabine
  • Interferon-gamma
  • Granzymes
  • Azacitidine