[In vitro regulation of HLA and B7 expression in multidrug-resistant breast cancer cells]

Di Yi Jun Yi Da Xue Xue Bao. 2002 Feb;22(2):107-10.
[Article in Chinese]

Abstract

Objective: To study the modulation of the expressions of human leucocyte antigen (HLA) and co-stimulatory molecules B7 (CD80, CD86) in multidrug-resistant (MDR) breast cancer cells.

Methods: The MDR phenotype MCF-7/ADR cells were treated with recombinant human interferon (IFN)-alpha2b (rhIFN-alpha2b) at different doses for varied length of time, and the expressions of HLA and B7 were determined by flow cytometry (FCM) and compared with those of non-treated cells. Statistical analysis was performed using SPSS10.0 software.

Results: At the doses smaller than 1x10(3) IU/ml, rhIFN-alpha2b did not exhibit significant inhibition on MCF-7/ADR cell growth, but HLA and B7 expressions were enhanced in a dose- and time-dependent fashion and significant up-regulation occurred 24 h after 400 IU/ml rhIFN-alpha2b treatment. Treatment with rhIFN-alpha2b at the doses of 100, 400, 800 IU/ml respectively for 24 h produced significant increases in the positive cell ratios for HLA class I expression (P<0.05), HLA-DR expression (P<0.005) and B7-2 expression (P<0.05), while changes in B7-1 expression was not obvious (P>0.05). The mean relative linear fluorescence intensity (RLFI) of HLA class I was also significantly increased (P<0.001) but alterations in the mean RLFI of HLA-DR and B7 were not significant.

Conclusions: rhIFN-alpha2b within the dose range from 400 to 800 IU/ml can effectively enhance the expression of HLA and B7 molecules, suggesting that it may have the potential to reverse immune tolerance of breast cancer cells. Cytokine treatment may be effective in reversing immune tolerance caused by down-expression of HLA and B7.

MeSH terms

  • Antigens, CD / metabolism*
  • B7-1 Antigen / metabolism*
  • B7-2 Antigen
  • Breast Neoplasms / metabolism*
  • Breast Neoplasms / pathology
  • Drug Resistance, Multiple / physiology*
  • Female
  • HLA Antigens / metabolism*
  • Humans
  • Interferon Type I / pharmacology
  • Membrane Glycoproteins / metabolism*
  • Recombinant Proteins
  • Tumor Cells, Cultured

Substances

  • Antigens, CD
  • B7-1 Antigen
  • B7-2 Antigen
  • CD86 protein, human
  • HLA Antigens
  • Interferon Type I
  • Membrane Glycoproteins
  • Recombinant Proteins